The Revenge of the Guinea Pigs

Dr. Michale Behe accepts data such as the GULO gene as evidence of common descent.

"creationists could have done this analysis of GULO genes themselves"

As if!

Fixed typo. Thanks!

YW! :-)

As I mentioned, the nested hierarchy of the broken version of the GULO gene is powerful evidence of common ancestry. The Guinea Pig also has a broken GLUO gene, but it is broken in a different way to the primate genes, and does not nest with them.

As can be clearly seen in the above diagram, the rat sequence has diverged from the ancestral sequences. So no mutational hotspots; Nishikimi was incorrect (and has admitted so in private correspondence). But that’s the good thing about science, it is self correcting, if we make mistakes, we fix them when new data comes out.

So, once again, we must ask the IDiots to "Go stick your head in a pig" ;-P

CDV said: Have there been published articles concluding that Nishikami was wrong ? My Pubmed search couldn't seem to find any, or I may have been choosing my keywords wrong. In the absence of the above, it would be helpful if Nishikami's more recent views, expressed privately in his correspondence, could be given as much publicity as his original study.

Try for a moment to think like someone who truly has a problem with common descent. Specifically, that you seriously thought various groups of animals (all eukaryotes) originated independently from nonliving matter. The first thing that you'd want to do is avoid weasel words like "common design" because how better to implement "common design" than by descent with (possibly radical) modification? Second, you'd avoid reference to design altogether, because a designer could actuate that design anyway he wanted. Even Richard Sternberg admits that. Third, you'd avoid finding weakness with "RM + NS" because, as Behe will tell you, that does not refute common descent. Fourth, you would avoid at all costs "improbability of abiogenesis" calculations, because your "theory" requires many abiogenesis events (of eukaryotes, no less), whereas common descent can accommodate a single, extremely rare event.

If your objection is only about common descent, you might also want to make it perfectly clear that you have no objection to the chronology of biological history that is agreed upon by many fields in science, not just evolution. And to further dispel any doubt that you are serious, you'd be very clear about when those new lineages arose from nonliving matter. Even if they were just tentative "best guesses," you'd assure us that you planned to test them, and reject them if necessary.

Lets also say that, like creationists and IDers, you don't conduct original research, but just sit on the sidelines and evaluate work done by others. What then would be your argument against common descent? Simple, you would analyse the hypotheses and conclusions of people like Schwabe, Senapathy and Goldschmidt, and argue why Goldschmidt is the odd man out. To further assure that your objection is strictly scientific, you'd challenge Behe directly - again with no reference to his design argument. And you'd never have to use the word "Darwinism."

Note, by "animals (all eukaryotes)" I mean "animals (all of which are eukaryotes)," not necessarily that you thought that every species of eukaryote originated independently.

You people really should ignore the YEC crowd, the creos arguing against common descent. It just mucks things up. I always ignore their nonsense; and I don’t have near the contempt for them that most neo-Darwinan atheists, and the occasional neo-Darwinian theist, have. Hell, some of my best friends are YECs. Just refer them to Behe, and forgetaboutit. If Behe can’t convince them, trust me, you neo-Darwinian atheists never will.

The only actual issue is how much evolution can actually be shown (preferably quantitatively rather than through just so stories) to have resulted from RM+NS. To those of us that don’t blindly accept the neo-Darwinan/Dawkins party line, most would bet our left testicle that beyond simple mutations that are almost always a degradation of sorts----and that result in things like microorganism drug resistance, human resistance to malaria,” Antarctic icefish “antifreeze” (and also the development of that HIV viral protein-vial protein binding site that Behe unfortunately overlooked when writing EoE, but has now acknowledged as having evolved apparently after RM+NS had around 10^20 shots at it, numbers similar to malaria’s CQ resistance), etc.----not much.

The only actual issue is how much evolution can actually be shown (preferably quantitatively rather than through just so stories) to have resulted from RM+NS. To those of us that don’t blindly accept the neo-Darwinan/Dawkins party line, most would bet our left testicle that beyond simple mutations that are almost always a degradation of sorts—-and that result in things like microorganism drug resistance, human resistance to malaria,” Antarctic icefish “antifreeze” (and also the development of that HIV viral protein-vial protein binding site that Behe unfortunately overlooked when writing EoE, but has now acknowledged as having evolved apparently after RM+NS had around 10^20 shots at it, numbers similar to malaria’s CQ resistance), etc.—-not much.

The only actual issue is how much evolution can actually be shown (preferably quantitatively rather than through just so stories) to have resulted from RM+NS. To those of us that don’t blindly accept the neo-Darwinan/Dawkins party line, most would bet our left testicle that beyond simple mutations that are almost always a degradation of sorts—-and that result in things like microorganism drug resistance, human resistance to malaria,” Antarctic icefish “antifreeze” (and also the development of that HIV viral protein-vial protein binding site that Behe unfortunately overlooked when writing EoE, but has now acknowledged as having evolved apparently after RM+NS had around 10^20 shots at it, numbers similar to malaria’s CQ resistance), etc.—-not much.

Tell us, bigbangBigot, why are gain-of-function mutations, both single and series of, considered "degradation"?

bigbang said: To those of us that don’t blindly accept the neo-Darwinan/Dawkins party line, most would bet our left testicle that beyond simple mutations that are almost always a degradation of sorts----and that result in things like microorganism drug resistance, human resistance to malaria,” Antarctic icefish “antifreeze” (and also the development of that HIV viral protein-vial protein binding site that Behe unfortunately overlooked when writing EoE, but has now acknowledged as having evolved apparently after RM+NS had around 10^20 shots at it, numbers similar to malaria’s CQ resistance), etc.----not much.

bigbang,

Arguing that evolution is theoretically impossible is futile. This evidence shows that it in fact did occur. What is your explanation for the nested hierarchy of genetic similarities shown in the phylogeny? Remember that this was drawn using pseudogene sequences. How do you account for the fact that this phylogeny is congruent with the relationships shown by every other data set? Why do you think that hand-waving arguments are more convincing that actual evidence?

that beyond simple mutations that are almost always a degradation of sorts—-

Microbes drive almost all chemical reactions in the ocean; it’s important to identify the specific professions held by different groups.

Polz and former graduate student Dana Hunt, now a postdoctoral researcher at the University of Hawaii, created a large and accurate genetic data set by isolating and identifying over 1,000 strains of vibrio bacteria from a sample of eight liters of seawater gathered near Plum Island, Mass., in the spring and fall.

“What is really new about our approach is that we were able to combine both molecular data (DNA sequences) with ecological data in a single mathematical framework,” said Alm. “This allowed us to solve the inverse problem of taking samples of organisms from different environments and figuring out their underlying habitats. In essence, we modeled the evolution of a microbe’s lifestyle over millions of years.”

Also the authors argue that these populations are efficiently separated,

Quoting from the head of the page: "Creatures inherit their DNA from their parents, who have inherited their DNA from their parents and so on into the past. We use this information to do paternity tests, and form genealogies. The nested hierarchy of DNA similarity is evidence that organisms descended from a common ancestor."

As a juvenile sitting in a classroom can see, the first sentence in that quote absolutely rules the final sentence out of all realms of possibility.
Or is someone going to explain why common descent doesn't equal "creatures inherit[ing] their DNA from their parents", said DNA enabling scientists "to do paternity tests"?

By definition of the "common descent" being called upon, the best that DNA might be able to do is enable scientists to attempt nested hierarchy membership tests, no certainty issuing therefrom. Your particular DNA might show you are a throwback to a wobbygong. But there is a rational alternative to this business of publicly walking about on the ceiling.

You people really should ignore the YEC crowd, the creos arguing against common descent. It just mucks things up. I always ignore their nonsense; and I don’t have near the contempt for them that most neo-Darwinan atheists, and the occasional neo-Darwinian theist, have. Hell, some of my best friends are YECs. Just refer them to Behe, and forgetaboutit. If Behe can’t convince them, trust me, you neo-Darwinian atheists never will.

— bigbang

PBH,

What is your explanation for the nested hierarchy of genetic similarities displayed in the phylogeny? Why does this data reveal exactly the same pattern as displayed in other data sets?

The Phoenix lander has successfully touched down on Mars.
http://www.nasa.gov/multimedia/nasatv/index.html

The lander carries a CD which includes the names of my children.

No images yet, but the lander is sending back telemetry and has landed somewhere flat "like a table" someone just yelled. Soon it will begin it's search for water.

D.S.,

Species were conduits of life, not blood ancestors. There is a total difference, but nevertheless it is easy to confuse the conduit notion with the ancestor notion.

When speciation occurred - it was instantaneous in terms of geologic time - DNA was adjusted/re-programmed, the species lock was tripped and a new lock was set, a new species immune system likewise had to be set, and so on. These are all things that are theoretically possible. Speciation itself presumably implicated genetic engineering and something approximating to surrogate motherhood, done via quantum category info. technology, operating in Nature. Again, theoretically possible.

The re-programming of the genetics (with total species information, in one hit) implicates more than one source of empowering and information input: the empowering signalling had something to do with celestial bodies, especially the sun-earth-moon system; but the observed modification in keeping with environmental requirements suggests information storage and retrieval in the information bank of the organism itself. On top of this we have the observed fact that planning capacity in the form of genes is passed on from species to species, which said capacity was activated by the onset of relevant environmental conditions.

So we have information capacity, we have information signalling, we have mechanisms that respond to readable signals, we have an increasing spread of genetic capability as evolution proceeds. Information, playing on a finite array of "keys", to produce music. Each species unique, because of the abundant permutations and combinations available. Each species suited in some ways to environment, because the inbuilt information reading/response capacity promotes it. All species having commonality of genetics, because they were evolved under the same info. tech. system which accessed the collection of genetic options available.

Conduits, not blood ancestors. Common Descent evolution is about equivalent to charting the North-West Passage in a timber ship, with lead food tins for the crew.

Given that the Earth coalesced in or with the assistance of something like water, probably H2O, itself, there is no reason why other planets might not have done the same.

Congratulations on this achievement. Can we hear the CD?

Philip Bruce Heywood said: Species were conduits of life, not blood ancestors. There is a total difference, but nevertheless it is easy to confuse the conduit notion with the ancestor notion.

Philip Bruce Heywood said: D.S., Species were conduits of life, not blood ancestors. There is a total difference, but nevertheless it is easy to confuse the conduit notion with the ancestor notion. When speciation occurred - it was instantaneous in terms of geologic time - DNA was adjusted/re-programmed, the species lock was tripped and a new lock was set, a new species immune system likewise had to be set, and so on. These are all things that are theoretically possible. Speciation itself presumably implicated genetic engineering and something approximating to surrogate motherhood, done via quantum category info. technology, operating in Nature. Again, theoretically possible. The re-programming of the genetics (with total species information, in one hit) implicates more than one source of empowering and information input: the empowering signalling had something to do with celestial bodies, especially the sun-earth-moon system; but the observed modification in keeping with environmental requirements suggests information storage and retrieval in the information bank of the organism itself. On top of this we have the observed fact that planning capacity in the form of genes is passed on from species to species, which said capacity was activated by the onset of relevant environmental conditions. So we have information capacity, we have information signalling, we have mechanisms that respond to readable signals, we have an increasing spread of genetic capability as evolution proceeds. Information, playing on a finite array of "keys", to produce music. Each species unique, because of the abundant permutations and combinations available. Each species suited in some ways to environment, because the inbuilt information reading/response capacity promotes it. All species having commonality of genetics, because they were evolved under the same info. tech. system which accessed the collection of genetic options available. Conduits, not blood ancestors. Common Descent evolution is about equivalent to charting the North-West Passage in a timber ship, with lead food tins for the crew.

Folks, don't feed trolls. And don't quote large amounts of other peoples text, it makes following the thread hard. Thanks for your consideration.

Philip Bruce Heywood said: Quoting from the head of the page: "Creatures inherit their DNA from their parents, who have inherited their DNA from their parents and so on into the past. We use this information to do paternity tests, and form genealogies. The nested hierarchy of DNA similarity is evidence that organisms descended from a common ancestor." As a juvenile sitting in a classroom can see, the first sentence in that quote absolutely rules the final sentence out of all realms of possibility. Or is someone going to explain why common descent doesn't equal "creatures inherit[ing] their DNA from their parents", said DNA enabling scientists "to do paternity tests"?

Scott said: I call Poe’s Law on PBH!

So then PBH, you have absolutely no explanation why the pattern observed in pseudogenes should correspond precisely to what is expected if common ancestry is true. Your incoherent mumblings do not even begin to address the issue and from what I can tell, your supposed hypothesis is completely inconsistent with the observed pattern. Why in the world would some "info tech system" produce the exact pattern expected from common ancestry in nonfunctional genes? Once again, all you have is wishful thinking.

Folks, don't feed trolls.

Oh, come on!

how long have you been contributing here, Ian?

In all that time, have trolls EVER been ignored?

No.

Like it or not, the onus is on YOU to remove the trolls from your thread to the BW.

I'm not even going to go into the many reasons why people respond to trolls, which you should also know by now.

Hey, Ian. I scooped you four years ago. I see that Paul Nelson is still peddling his "interpretation" after I corrected him way back when.

Common Design Errors

Scurvy, Guinea Pigs, and You

What is Poe's Law?

Rilke's- Granddaughter-Who-Is-Less-HOMO sapiens-Than-Grandparents (according to Common Descent) mustn't have bumped into my publications. Observe, Oh Descendant of the honorable Rilke, that the others aren't asking me to quote facts and give references. They are apprehensive, because they know I can do so. I am not about to regurgitate my readily available publications herewith. As the Page Host points out, some repetition is unnecessary. One could try the link that is my name. But almost every day, publications such as SCIENCEDAILY tell the story. I will shortcut you to one SCIENCEDAILY article in particular. It's linked to via my site, and I have forgotten the link details, but you could search under HOX GENES - PADDLEFISH - TETRAPODS in the not-very-old archives. Paddlefish pre-date tetrapods, yet they have genes that theoretically will activate to build arms and legs if suitably triggered. The new discoveries re. species lock, quantum info.tech. and all the paraphernalia - it's all there. And I predicted some of it. You could do the same, by applying logic.

I'm interested in this PHOENIX Lander.

Reed A. Cartwright said: Hey, Ian. I scooped you four years ago. I see that Paul Nelson is still peddling his "interpretation" after I corrected him way back when. Common Design Errors Scurvy, Guinea Pigs, and You

I see that Paul Nelson is still peddling his "interpretation" after I corrected him way back when.

all the IDiots are firm believers in the "a lie told often enough" method of communication.

especially if that lie sounds plausible to the target audience.

Ian Musgrave said: Folks, don't feed trolls. And don't quote large amounts of other peoples text, it makes following the thread hard. Thanks for your consideration.

Philip Bruce Heywood said: What is Poe's Law? Rilke's- Granddaughter-Who-Is-Less-HOMO sapiens-Than-Grandparents (according to Common Descent) mustn't have bumped into my publications.

Observe, Oh Descendant of the honorable Rilke, that the others aren't asking me to quote facts and give references.

The new discoveries re. species lock, quantum info.tech. and all the paraphernalia - it's all there. And I predicted some of it. You could do the same, by applying logic.

Why keep blathering on?

*psst*

he's nuts.

Ichthyic said: Why keep blathering on? *psst* he's nuts.

Really?

really really.

still, don't take my word for it, of course.

you can scroll back on his many missives here and judge for yourself.

you'll find about a 10:1 ratio of insane gibberish to sensibility.

...btw, how is post-doc life treating you these days?

where did you end up?

Dear Dr Musgrave,

Royal Truman and I recently published the complete genetic analysis of the GULO exon X (J Creat 2007, 21 (3): 118-127). It is similar to yours, but you also miss some obvious conclusions. It turned out both darwinist's and creationist's interpretations were wrong. The indel on position 97, however, can still be interpreted a non-random position.

Further, you take nested hierarchy as evidence for common descent, but you fail to recognize the evidence against common descent: genetic novelties in protein coding and RNA genes. Humans have unique genes, such as HARs, which did not evolve in a Darwinian way (by mutation and selection that is). 1% of the human genome is unique. That is sufficient to overturn common descent. It should prompt us to think about alternatives instead of pushing the data in a falsified paradigm.

Nested hierachy can easily be falsified on the gene level. Increasingly, HGT and loss of never observed duplicates have to be invoked to "explain" aberrant data. It's nothing but phlogiston.

Considering your hapothetical schema above. Did you already tune in on the platypus genome published last month? What do you make of it? It tells me Darwinian evolution can be thrown out. But that's not new, I already knew that because of genetic redundancy and the no-phenotype knockout.

The big mistake is common descent from a SINGLE ancestor. This vision was falsified several years ago, so let it go, Darwinians. Get used to the idea there is common desnent from many ancestors. In an atheist framework that is not allowed. Darwinism has simply become the religion of the atheists. The evo-crea discussion is not a scientific one. You and I know that.

Regards,

Peter

It turned out both darwinist's and creationist's interpretations were wrong.

Further, you take nested hierarchy as evidence for common descent, but you fail to recognize the evidence against common descent: genetic novelties in protein coding and RNA genes. Humans have unique genes, such as HARs, which did not evolve in a Darwinian way (by mutation and selection that is).

1% of the human genome is unique. That is sufficient to overturn common descent.

Nested hierachy can easily be falsified on the gene level. Increasingly, HGT and loss of never observed duplicates have to be invoked to "explain" aberrant data.

Considering your hapothetical schema above. Did you already tune in on the platypus genome published last month? What do you make of it? It tells me Darwinian evolution can be thrown out.

In an atheist framework that is not allowed. Darwinism has simply become the religion of the atheists. The evo-crea discussion is not a scientific one. You and I know that.

Your comments are irrelevant to address my points.

My science education tells me when a hypothesis is no longer tenable. Contemporary biology has shown beyond any doubt Darwin was wrong, the evolutionary paradigm fallen. I set up an entiry novel biology that expalins where Darwin fails. It was quite a project but now it is there. Simply screen for GUToB.

"My explanations are better because they explain better"

;)

"Descent with modification. Descent with modification. How many times must this be pointed out?"

No, my dear, design with novelties. How many times do we have to spell out: DESIGN WITH NOVELTIES is what biology shows, not descent with modification. How doe you modify an entire novel gene? Humans have 36 unique protein coding genes. And we don't know yet how many unique small regulatory RNA genes (because it was all "junk" according to the Darwinists outdated thinking. Due to their simplistic 19th century paradigm science lags ten years behind).

We can, if you wish, discuss the HAR1F region. Or additional unique sequences in humans. I went this lane 1000 times and never lost a single discussion. It's going to be a sure case for me. I only have to copy and paste from my archive.

Just let me know how you want me to falsify Darwin. I have examples ready to obliterate Darwin, selection mechanism, common descent, Ohno, whatever.

Well good God, man! Go publish your earth-shaking research in a peer reviewed scientific journal and claim you Nobel!

"Look, you are the one who didn't seem to understand how the journal system works. You are the one who didn't understand that the position of the foramen magnum in fossil primate skulls indicated how upright the individual walked. You are the one who has repeatedly cited journal articles as support for your position when it is clear that the articles do not support your position at all. In fact, you seem to not even read the articles carefully, or at all, before you cite them. You are the one who thinks that inference doesn't happen in science, when that is precisely how all science is conducted; by making inferences."

Further, you take nested hierarchy as evidence for common descent, but you fail to recognize the evidence against common descent:

— peter borger, biologist, PhD

Just let me know how you want me to falsify Darwin.

— peter borger, biologist, PhD

peter borger, biologist, PhD said: Dear Dr Musgrave, Royal Truman and I recently published the complete genetic analysis of the GULO exon X (J Creat 2007, 21 (3): 118-127). It is similar to yours, but you also miss some obvious conclusions. It turned out both darwinist's and creationist's interpretations were wrong.

The indel on position 97, however, can still be interpreted a non-random position.

Damian said: For anyone who doesn't know who Peter Borger is, he is most certainly not a PhD Biologist. Peter Borger is a Postdoctoral Fellow in the Department of Pharmacology at the University of Sydney according to this, although it is several years old. He also appears to be a creationist.

peter borger, biologist, PhD said: How doe you modify an entire novel gene?

Ian Musgrave said: SFX: Polite cough
Sorry, but we Pharmacologists are biologists, the vast majority of us understand evolution and have a modest working knowledge of phylogeny (we receptorologists are prone to making phylogenetic trees of our receptors, and kinases and .. almost anything really). Yep, Dr. Borger is a PhD biologist in Pharmacology, an expert in asthma who is now at the University Hospital of Basel, Switzerland. He doesn't have a clue about evolutionary biology though.

Your comments are irrelevant to address my points.

My science education tells me when a hypothesis is no longer tenable. Contemporary biology has shown beyond any doubt Darwin was wrong, the evolutionary paradigm fallen. I set up an entiry novel biology that expalins where Darwin fails. It was quite a project but now it is there. Simply screen for GUToB.

My explanations are better because they explain better

For anyone who doesn’t know who Peter Borger is, he is most certainly not a PhD Biologist. Peter Borger is a Postdoctoral Fellow in the Department of Pharmacology at the University of Sydney according to this, although it is several years old. He also appears to be a creationist.

I have to admit to a profound sense of sadness in realizing that someone who is clearly a competent scientist (though, not in the relevant field, of course) spends his timing childishly bragging about how he can “falsify Darwin” – on websites of all places – rather than remaining faithful to his scientific training and actually publishing his “findings”.

"Dr. Borger is a PhD biologist in Pharmacology" & "he is most certainly not a PhD Biologist. Peter Borger is a Postdoctoral Fellow in the Department of Pharmacology at the University of Sydney"

Wrong. Dr Borger is a Dutch molecular biologist, specialized in regulation of eukaryotic gene expression in particular in humans. He is antiDarwinian and he set up the GUToB theory.

You ask: "Which current and extinct lineages are the products of independent origin of life events?"

Many and I know how to determine this: genetic indicators.

The Cai & Zhao paper is on preexisting genetic elements. It's irrelevant.

If unique genetic elements prevent evolution from occurring, then why do we see it still occurring in everything from evening primroses to humans? Isn't that like claiming that fire does not burn while standing in a burning house?

"On the basis of genome comparison among yeast species, we have identified a new de novo protein-coding gene, BSC4 in Saccharomyces cerevisiae. The BSC4 gene has an open reading frame (ORF) encoding a 132-amino-acid-long peptide, while there is no homologous ORF in all the sequenced genomes of other fungal species, including its closely related species such as S. paradoxus and S. mikatae. "

Completely conform GUToB: all current Saccharomyces species resulted from one single baranome (Saccharomyces bn) which contained all information currently found in the seperate species. The baranome shuffled throwing up some reprodcutive barriers and hence S. Paradoxus and S mikatae arose (plus the other six or seven S. species). This socalled novel gene is in fact old frontloaded information that is redundnat in most environments and only S. cerevisiea was able to retain (probably due to nat sel). It is exactly what I predicted in my manuscript. Thanks for the link.

Come on guys, this one was easy.

GUToB makes biology easy.

If unique genetic elements prevent evolution from occurring, then why do we see it still occurring in everything from evening primroses to humans?

Due to VIGES (= variation inducing genetic elements). VIGEs are what mainstreamers call ERVs, LINEs, SINEs, ALUs, transposons, etc. Their positions affect gene regulation (even at far distance) and morphogenetic programs. They induce variation from the frontloaded baranomes by swapping genetic information, fascilitate duplications, disuption of (redundant) genes, position effects, etc. The variation which we observe in nature is actively generated from inside. Selection does not really play a role when it comes to formation of new species.

Further there is the illusion of common descent. The illusion is generated by the non-random nature of mutations. We know there are hotspots in DNA, we only did not realize they were so common and most of them have already changed in the past. Hence we get an almost perfect illusion of CD (and nested hierarchy). The location where a mutation is introduced is largely determined by the DNA sequence and can be predicted. I can predict with reasonable accuracy where mutations will be introduced in a sequence using my newly developed methods. I can also demonstrate that it is very likely the indel on position97 in the GULO exon X of primates is due to a mechanism.

In conjunction with functional constraints of proteins (phosphorylation sites, ubiquination sites, sumoylations ites, docking sites, etc, etc), NRM create the genetic mirrage of common descent.

So, Borger did a 'complete genetic analysis' with his YEC chemist pal...

Oh, wait -a 'complete' analysis of one exon of one gene, and wants to overturn evolution.

How typical.

This, of course, is the creationist asthma researcher who has claimed that partial exon data from one gene supercedes 10+ kb of data. Who has claimed that there are magical particles - undiscoverered, of course - called "creatons." Who has claimed that some mutations are so non-random so as to appear random.

But he thinks that appending "PhD" to his name renders his, frankly, idiotic claims irreproachable.

Just another Dunning-Krugwer creationist.

peter borger, biologist, PhD said: Completely conform GUToB: all current Saccharomyces species resulted from one single baranome (Saccharomyces bn) which contained all information currently found in the seperate species. The baranome shuffled throwing up some reprodcutive barriers and hence S. Paradoxus and S mikatae arose (plus the other six or seven S. species). This socalled novel gene is in fact old frontloaded information that is redundnat in most environments and only S. cerevisiea was able to retain (probably due to nat sel). It is exactly what I predicted in my manuscript. Thanks for the link. Come on guys, this one was easy. GUToB makes biology easy.

The implications for the data Penny's article refers to: 1) all genetic changes are fast, not slow [1], 2) we cannot have an common ancestor with chimps 5-6 million years ago [1], 3) darwin was wrong, 4) the darwinians are wrong, 5) currently we do not have a evolutionary theory. [1] Penny asks why nobody noticed this paradox before. This is untrue. Several creationists have pointed it out. Four years ago I have demonstrated this on the EvC board. I have tried to get in published in the scientific (darwin-minded) literature, without success. Now darwinians cannot longer obscure what is obvious they produce papers such as Penny's. With their dogmas the Darwinians are not only blocking the truth, they also block scientific progress (Over the last decade at least five years have been lost).

Anybody for a clear-cut falsification of common descent at the molecular level? I know many so please let me know if you are interested in a demonstration.

Peter,

How do you explain the nested hierarchy of genetic similarities shown in the phylogeny? Why does it give the exact same answer as every other data set?

Why do you think that it is necessary to observe the intermediate stages of every gene duplication event in order to infer the origin of new genes? You do know that many gene duplications have been observed don't you?

Why do you think that finding a few "novel" genes invalidates common descent? Why is the nested hierarchy still found in the other genes? Why is the nested hierarchy found in pesudogenes and SINE insertions? Have you found any organisms that have no genetic similarity to any other organisms? Have you found any genes that could not have peen produced by gene duplication and divergence? Do you have any alternative explanation for the origin of species? DO you have any evidence for this hypothesis?

You naughtly little selector. And that only after four mails!

Could you please show my interpretation of the Cai and Zhoa paper and comment to that. It would suit you as a scientist. If not...

...go and look in the mirror, look into your own eyes and ask yourself: who am I.

regards,
Peter

peter borger, biologist, PhD said: Could you please show my interpretation of the Cai and Zhoa paper and comment to that.

Borger has a well documented history of taking quite literally tiny bits of data and wildly extrapolating it inot grand proclamations. I've been reading through his forays at the more or less defunct ISCID site, and he rambles on about falsifying 'Darwinism' via data from single exons, single parts of loci, etc.

I am reading one hilarious thread over there now from 2006 in which he is arguing that because the intraspecific variation in part of the human cytochrome c sequence is greater than the interspecficic variation between human and chimp, then surely, evolution is all wrong.

Tell us all, PeeBee, how many individuals are typically used when making interspecies comparisons?

Some things never change...

Found those 'creatons' yet?

LOL!

Ian Musgrave notes: “the ability of bacteria to breakdown nylon, pentacholophenyl and atrazine are due to the development of new enzymes.”

.

Hey Doc, thanks for responding. When asked if the “evolution of nylonase in two different strains of flavobacterium and of pseudomonas aeruginosa was a good example of an increase of information in the genome; and whether it refuted the main contention of his book,” Behe replied: “No. Those enzymes are very simple ones which simply hydrolyze precursors to nylon. That’s a very simple task, which can be done even by small organic catalysts.”

.

Ian Musgrave said: “The HIV Vpu ion channel evolved after much less than 10^20 “shots” as you call them, see my open letter part 6 where I discuss how Behe has gone badly wrong in detail.”

In letter 6 Ian Musgrave writes: “I would like to note that both your [Behe’s] mutation rates (10^-4) and effective population size (10^9 to 10^10) are too high. By a factor of around a hundred thousand,.” And that “In considering mutational effects, and generating new mutations, you need to consider the effective population size,” noting that “It’s been estimated to be between 10^3 and 10^5 (depending on the kinds of assumption you make[1]).”

.

Regarding the mutation rate, you suggest 10^-5+, but then graciously concede “what’s a half log unit between friends?”----so apparently estimated mutation rate differences don’t concern you all that much.

Regarding the effective population estimate, you note there are various estimates; 10^3 and 10^5 depending on the assumptions you make, compared to Behe’s 10^9-10^10. Well, OK, depending on the assumptions, but then there will always be an effective population rate problem, depending on assumptions, in all populations, including the estimated 10^40 cells that RM+NS has had to tinker with during earths 4 billion year history; suggesting that perhaps RM+NS actually had much, much less than the 10^40 cells to work with?

And keep in mind that, as Behe notes, the title of his book is The Edge of Evolution. He clearly acknowledges RM+NS can do some things, but not others (along with many others that don’t buy ID), and he’s only attempting to find a rough dividing line.

I still find that Behe’s arguments (including the 10^20 number), evidence, and skepticism regarding what RM+NS can and can't actually accomplish, a bit more convincing than the typical neo-Darwinian’s faith in RM+NS. Nevertheless, if you neo-Darwinians ever come up with something as convincing as, say, the BB has been for cosmological theory, I’ll gladly rethink my position (besides, my left testicle hasn’t been functional for decades . . . thank God that he and/or RM+NS provided me with two).

1% of the human genome is unique. That is sufficient to overturn common descent.

"How do you explain the nested hierarchy of genetic similarities shown in the phylogeny? Why does it give the exact same answer as every other data set?"

First of all what answer do you want to have? One that is conform the paradigm, I presume. And you will have it: There is no alternative to Darwinism in naturalistic philosophy. More and more genes are not in line with it, however. I discussed the cyt c gene as an example years ago, and I showed, it is even admitted, some sequences are excluded in phylogenies because they upset the tree. In the meantime it has become worse. An entire disciplin is dedicated to genetree-reconsiliation. They add and subtract genes as if these guys do math. And we have of course HGT? For what reason? Too keep up the paradigm. Chimps and humans are sometimes the closest relatives, sometimes chimps and gorilla or sometimes humans and gorilla. The reason? Homoplasy. What does it mean? Nothing besides that the sharing of a sequence. You are relying on statistics , selfinvented models and meaningless words to get it all in line with what you expect from theory. If that is science creation science is science.

One single aberrant gene (we have discovered many) is sufficient to turn over the hypothesis. But that will not happen, since what you study is true from the start. This is the axioma of evolutionary theory: Evolutionary theory is true. Why do you guys still do evolutionary research? You know all the answers upfront. That's not science. That's pseudoscience I do not want to be involved in.

We find aberrant genes everywhere. Some genes do not show any expected pattern. Then you guys come with ad hoc hypotheses to "explain" the data, unaware apparently you've left the scientific method long ago. Science proceeded by falsifying observations. If it doesn't matter anymore what we observe, why do science?

That's the point: it doesn't matter what we observe everything fits the paradigm. It's the other way around, mates, and because Darwinism (although he had some pretty good ideas) has been hijacked by the atheists I decided to join the other camp.

You should read outside the Darwinian literature. The pope is not going to tell you Christ doesn't exist (I am not sure about the pope, however).

O, you already know evolution is true? That's what I mean.

Anybody for the HAR1F gene, that beuatiful human-specific regulatory RNA gene that defies a Darwinian explanation?

Just let me know by mail: peterborger@hotmail.com

And you will have a personal answer.

PS: Scott Page, it is worse for the paradigm now than it was in the "good old days" when we were suspended together from the EvC forum. Remember? Cheers mate. (No hard feelings, just good old bodies with distinct opinions)

Well that's three for three. I asked every one of these guys to explain the pattern observed and not one could do it.

The nested hierarchy is consistent in different data sets for both functional and nonfunctional genes and corresponds precisely to the fossil record as well. This is very strong evidence for common descent.

Arguing that it couldn't have happened explains nothing. Arguing that some mysterious unobserved process is involved explains nothing. Arguing that that there might be some things that are not yet fully explained is of course irrelevant and also explains nothing.

Then of course there is the problem of coming up with an alternative explanation that better explains the observed pattern. No one seem to be able to do that either. So I guess modern evolutionary theory and descent with modification is still the best explanation for the observed pattern.

That’s the point: it doesn’t matter what we observe everything fits the paradigm.

"For humans we have a reasonable fossil record going back 4 million years. The further back in time one goes, the less like us the fossils look. Until one gets to Australopithecines like lucy. That humans were created suddenly on a saturday 6,000 years ago is not in accord with the facts."

I am biologists and what biology tells me is not in accord with the Darwinian paradigm. I can't judge whether or not the earth is old, or young, I know that genetic redundancy (a trait of all extant organism) brings doubt upon several evolutionary beliefs:

1) GR is not associated with genetic duplications,
2) redundant genes (RG) do not mutate faster than essential genes,
3) GR are not subject to purifying selection.cannot reside in the genome for ages since RG are

Ohno down, Kimura down, Darwin down. That's a lot for a single observation: no-phenotype knockouts.

That's the state of the art biology, my dear friends.

Better come up with some real explanations.

come on guys,

if you don't want to discuss the interesting topic of biology why do you all post here?

If you think you have a question don't hesitate to contact me:

peterborger@hotmail.com

All the best,
PB

That’s the state of the art biology, my dear friends. Better come up with some real explanations.

If you want to read about Borger's story

“The HAR1F gene: a Darwinian paradox.” Journal of Creation 21, No. 3 (2007) p55-57

Of course in the Dutch newspaper "De Volkskrant" Peter Borger blogs about this gene, reminding us that the 300 million years are just 'imaginary evolution years'.

Fascinating we have a Young Earth Creationist amongst us. As an EX-YEC'er I feel his pain. No wonder he sounds so 'convinced' yet somewhat confused about the facts.

peter borger, biologist, PhD said: "For humans we have a reasonable fossil record going back 4 million years. The further back in time one goes, the less like us the fossils look. Until one gets to Australopithecines like lucy. That humans were created suddenly on a saturday 6,000 years ago is not in accord with the facts." I am biologists and what biology tells me is not in accord with the Darwinian paradigm. I can't judge whether or not the earth is old, or young, I know that genetic redundancy (a trait of all extant organism) brings doubt upon several evolutionary beliefs:

I will actually be curious to see if Borger can produce ANY coherent explanation of why he thinks redundancy is a problem for evolutionary theory. I've never seen a creationist make an intelligent argument. Perhaps Dr. Borger can be the first?

Rilke's Granddaughter said: I will actually be curious to see if Borger can produce ANY coherent explanation of why he thinks redundancy is a problem for evolutionary theory. I've never seen a creationist make an intelligent argument. Perhaps Dr. Borger can be the first?

You ask: “Which current and extinct lineages are the products of independent origin of life events?” Many and I know how to determine this: genetic indicators.

— peter borger

I am biologists and what biology tells me is not in accord with the Darwinian paradigm. I can’t judge whether or not the earth is old, or young, I know that genetic redundancy (a trait of all extant organism) brings doubt upon several evolutionary beliefs:

PS: Scott Page, it is worse for the paradigm now than it was in the “good old days” when we were suspended together from the EvC forum. Remember? Cheers mate. (No hard feelings, just good old bodies with distinct opinions)

The problem with creationists is that they object to a nested hierarchy a priori because of a religious belief that in their interpretation contradicts with the data. As is with radiometric dating, creationists refuse to explain or address the massive consistent data and instead focus on some minor data which they claim is irreconcilable with an old earth. Invariably their conclusions are based on flawed assumptions, inappropriate methods, contamination but that's not my focus right now. In both cases, radiometric dating and phylogenetic data, the data are incredibly consistent across different methods and consistent with other known data.

That’s the point: it doesn’t matter what we observe everything fits the paradigm. It’s the other way around, mates, and because Darwinism (although he had some pretty good ideas) has been hijacked by the atheists I decided to join the other camp.

The problem Borger is that one can simply search for your past forays and see how confused and arrogant you are on these issues. You have stated in the past that you are out to battle the ‘nihilism’ of evolutionists and such. Your mission seems to have taken over your common sense and your ability to understand scientific issues.

— Scott Page

peter borger, biologist, PhD said: The big mistake is common descent from a SINGLE ancestor. This vision was falsified several years ago, so let it go, Darwinians. Get used to the idea there is common desnent from many ancestors. In an atheist framework that is not allowed. Darwinism has simply become the religion of the atheists.

No, my dear, design with novelties. How many times do we have to spell out: DESIGN WITH NOVELTIES is what biology shows, not descent with modification. How doe you modify an entire novel gene? Humans have 36 unique protein coding genes.

Rilke's Granddaughter said: I will actually be curious to see if Borger can produce ANY coherent explanation of why he thinks redundancy is a problem for evolutionary theory. I've never seen a creationist make an intelligent argument. Perhaps Dr. Borger can be the first?

No, my dear, design with novelties. How many times do we have to spell out: DESIGN WITH NOVELTIES is what biology shows, not descent with modification. How doe you modify an entire novel gene? Humans have 36 unique protein coding genes. And we don’t know yet how many unique small regulatory RNA genes (because it was all “junk” according to the Darwinists outdated thinking. Due to their simplistic 19th century paradigm science lags ten years behind).

I am biologists (sic) and what biology tells me is not in accord with the Darwinian paradigm. I can’t judge whether or not the earth is old, or young...

— peter borger

bigbang said: Regarding the mutation rate, you suggest 10^-5+, but then graciously concede “what’s a half log unit between friends?”----so apparently estimated mutation rate differences don’t concern you all that much.

Fascinating we have a Young Earth Creationist amongst us.

— PvM

As an EX-YEC’er I feel his pain. No wonder he sounds so ‘convinced’ yet somewhat confused about the facts.

— PvM

I am very busy at the moment. For my friends I am always there, however. For urgent and serious questions about how to understand biology in the 21st century please send a mail to:

peterborger@hotmail.com

Thanks, mates.

Peter Borger wrote:We can, if you wish, discuss the HAR1F region.

Peter Borger wrote: What you missed in the literature (and what I did not miss because I am in the medical field) is that there are no real orphan genes.

Peter Borger wrote: The indel on position 97, however, can still be interpreted a non-random position.

Peter Borger wrote:Anybody for the HAR1F gene, that beuatiful human-specific regulatory RNA gene that defies a Darwinian explanation?

peter borger, biologist, PhD said: I am very busy at the moment. For my friends I am always there, however.

For urgent and serious questions about how to understand biology in the 21st century please send a mail to:

After Jesus talked to the multitude, people were eager to learn from him, to touch him and to be be healed by him. They followed him in huge numbers. It was because of his gentle and loving and caring attitude.

How are you guys talking evolutionary theory to the people? What are you going to teach them? Survival of the fittest? Natural selection? Vanity? Purposelessness?

I will tell you something: Evolutionary theory will never get anywhere. People will not listen to you (except of course the atheists) because you have nothing to offer them. In addition to that my interpretation of biology is right, my interpretations of biology makes sense to people as it implies a purposeful universe. That's what mankind is looking for. Purpose.

Don't you guys get it? Listen carefully, and behold, I will only say this once:

By your own standards: you can't win the debate. Why not? Because you are fighting an evolutionary process. Got that? It is an unstoppable process for ever ongoing (you say so). And you all believe it, isn't it?

I find it rather funny and also inconceivable that you guys don't understand you will never beat an evolutionary process. How can you beat a meme that was favoured by natural selection? The strongest power in the universe (you say so). You cannot beat the greatest power in the universe (I know). That's why you cannot and will not win the debate, even if you were right, by your own standards you will loose. So, better invest your energy elsewhere. Multiply and be fruitful, or something like that.

It's amazing you guys don't even understand your own pet theory and why you will loose the debate.

Why do I always feel so very sorry for you, my brothers?

In His service,

Peter

That all folks,

Ciao and have a good one.

Ian, if you are really interested you can mail me here:

peterborger@hotmail.com

Evolutionary theory will never get anywhere. People will not listen to you (except of course the atheists, and vast majorities in Western Europe, Canada, Japan...)

Wow, he gave up easily. Most cranks hang around for at least 1000 posts. Lightweight.

Did anyone else notice that Mr Borger failed, yet again, to explain how evolution/natural selection is an "illusion," despite the fact that people have been observing and manipulating this "illusion" for extremely tangible benefits for the last 9 to 12 millenia?

MartinM said:

Evolutionary theory will never get anywhere. People will not listen to you (except of course the atheists, and vast majorities in Western Europe, Canada, Japan, or the Vatican...)

Fixed.

Dr. Musgrave says: “Sarcasm, learn to recognize it.”

.

Works both ways Doc. Thanks again.

.

PvM says: “As an EX-YEC’er I feel his pain…”

.

Well, that certainly was a blind spot that you are at least now aware of. Good for you. But is that any reason to throw out baby Jesus with the bath water?

Consider that you may just have jumped from one foolish notion, YEC, to yet another, that all of life is ultimately the result of evolution via RM+NS (requiring, by Koonin’s reckoning, an infinite multiverse).

Ian,

if you doubt the Schmid and Tautz (S&T) data on Drosophila in the PNAS, you should send them a letter. I did but they did not accept it (for obvious reasons). As you know (not?) S&T set up a screen for fast evolving genes, but they missed non-random mutations in the IG5 gene. That observation simply provided the first evidence for my thesis that..

"..some mutations are non-random with respect to position and or nucleotide and produce, in conjunction with functional contraints of the protein design, an illusion of common descent (CD)."

Over the past 5 years evidence for non-random mutations accumulated. My second thesis holds that..

"..phylogeneticist study the illusion of CD and try to make sense of it in a false framework".

This is obvious from violations of gene trees all over, ad hoc hypotheses such as HGT (never observed in the organisms where it has to be invoked) or the novel disciplin of gene-reconsiliation (i.e. addition and subtraction of hypothetical duplications) to keep up the appearance of CD.

Phlogiston was a better theory.

It is exactly what Truman and I showed for the indel on poistion 97 in Exon X of the GULO gene (you can get the article for free at the CMI if you ask).

Shared mistakes in pseudogenes? Non random mutations!

Wow, that's new!

Yep, it is ground breaking. Earth shaking.

Feel it?

Not? Fundamentalist Darwinian!

Science commits suicide when it adopts a creed. Who said that?

peter borger, biologist, PhD said: I will tell you something: Evolutionary theory will never get anywhere. People will not listen to you (except of course the atheists) because you have nothing to offer them.

HAHAHA I knew it. In crankspeak, "goodbye" means "I'll be lurking to respond to any responses".

Listen, crank, science isn't about the search for purpose. It's just information. What you do with that information is up to you. You choose to distort it and lie about it.

fnxtr said: HAHAHA I knew it. In crankspeak, "goodbye" means "I'll be lurking to respond to any responses". Listen, crank, science isn't about the search for purpose. It's just information. What you do with that information is up to you. You choose to distort it and lie about it.

Peter Borger is Dutch, but his last known address is in Basel. His PhD thesis is not referenced as Biology but as Medicine. Given he does not know the simplest things on evolution - for instance, what random mutation means - this medicine background is not surprising.

PB writes prolific on any website, in any language.

The same discussion about GULO can be found on Gert Korthof's Dutch blog: http://evolutie.blog.com/2534762/#cmts.

Peter Borger hopelessly confused: How are you guys talking evolutionary theory to the people? What are you going to teach them? Survival of the fittest? Natural selection? Vanity? Purposelessness?

peter borger, biologist, PhD said: It is exactly what Truman and I showed for the indel on poistion 97 in Exon X of the GULO gene (you can get the article for free at the CMI if you ask). Shared mistakes in pseudogenes? Non random mutations! Wow, that's new! Yep, it is ground breaking. Earth shaking. Feel it? Not? Fundamentalist Darwinian! Science commits suicide when it adopts a creed. Who said that?

peter borger, biologist, PhD said: After Jesus talked to the multitude, people were eager to learn from him, to touch him and to be be healed by him. They followed him in huge numbers. It was because of his gentle and loving and caring attitude. How are you guys talking evolutionary theory to the people? What are you going to teach them? Survival of the fittest? Natural selection? Vanity? Purposelessness? I will tell you something: Evolutionary theory will never get anywhere. People will not listen to you (except of course the atheists) because you have nothing to offer them. In addition to that my interpretation of biology is right, my interpretations of biology makes sense to people as it implies a purposeful universe. That's what mankind is looking for. Purpose. Don't you guys get it? Listen carefully, and behold, I will only say this once: By your own standards: you can't win the debate. Why not? Because you are fighting an evolutionary process. Got that? It is an unstoppable process for ever ongoing (you say so). And you all believe it, isn't it? I find it rather funny and also inconceivable that you guys don't understand you will never beat an evolutionary process. How can you beat a meme that was favoured by natural selection? The strongest power in the universe (you say so). You cannot beat the greatest power in the universe (I know). That's why you cannot and will not win the debate, even if you were right, by your own standards you will loose. So, better invest your energy elsewhere. Multiply and be fruitful, or something like that. It's amazing you guys don't even understand your own pet theory and why you will loose the debate. Why do I always feel so very sorry for you, my brothers? In His service, Peter

That’s what mankind is looking for. Purpose.

Evolutionary theory is critical in medicine and agriculture.

So, 2% of life is designed? Which 2%? How do you know?

You read like the poster that was here recently insisting we "math it out", whatever that means.

RotundOne said:

Evolutionary theory is critical in medicine and agriculture.

Well of course 98% of the theory is very useful and correct. But there are parts that have not been validated or do not really work out. These are the parts that many think should be looked at with a different point of view. Just as Newtonian physics explained 99% there still was a little that did not work. And if we do not allow criticism of the theory will never find out the whole story.

fnxtr said: So, 2% of life is designed? Which 2%? How do you know? You read like the poster that was here recently insisting we "math it out", whatever that means.

These are the parts that many think should be looked at with a different point of view. Just as Newtonian physics explained 99% there still was a little that did not work. And if we do not allow criticism of the theory will never find out the whole story.

Borger asks: “How are you guys talking evolutionary theory to the people? What are you going to teach them?”

.

Koonin’s infinite multiverese, my YEC friend, a multiverse where all things are not only possible, but inevitable, including your young earth and their neo-Darwinism. Oh happy day.

Pim makes an excellent point. The claim that criticism of evolution is not permitted is, to be blunt, an incredibly stupid lie: easily disproved and logically absurd. Criticism of the theory occurs ALL THE TIME. The theory (or, as RBH has pointed out, the combination of theories) is tested every single time we find a new fossil or sequence another genome or even find a new species.

The theory is always being tested, examined and criticized. But that's not what IDiots want. They want their own unproved, unspecific, unfalsifiable conjecture taught as a valid, scientific alternative. And they want to do this WITHOUT HAVING DONE ANY ACTUAL SCIENTIFIC WORK.

That's the basic lie that IDiots are offering; "teach our conjecture, but we don't have to do any real work to support it."

That's why the claims of Expelled are so laughable and false.

RotundOne said:

Evolutionary theory is critical in medicine and agriculture.

Well of course 98% of the theory is very useful and correct. But there are parts that have not been validated or do not really work out. These are the parts that many think should be looked at with a different point of view. Just as Newtonian physics explained 99% there still was a little that did not work. And if we do not allow criticism of the theory will never find out the whole story.

RotundOne said:

Evolutionary theory is critical in medicine and agriculture.

Well of course 98% of the theory is very useful and correct. But there are parts that have not been validated or do not really work out. These are the parts that many think should be looked at with a different point of view. Just as Newtonian physics explained 99% there still was a little that did not work. And if we do not allow criticism of the theory will never find out the whole story.

Rilke's Granddaughter said: Pim makes an excellent point. The claim that criticism of evolution is not permitted is, to be blunt, an incredibly stupid lie: easily disproved and logically absurd. Criticism of the theory occurs ALL THE TIME. The theory (or, as RBH has pointed out, the combination of theories) is tested every single time we find a new fossil or sequence another genome or even find a new species. The theory is always being tested, examined and criticized. But that's not what IDiots want. They want their own unproved, unspecific, unfalsifiable conjecture taught as a valid, scientific alternative. And they want to do this WITHOUT HAVING DONE ANY ACTUAL SCIENTIFIC WORK. That's the basic lie that IDiots are offering; "teach our conjecture, but we don't have to do any real work to support it." That's why the claims of Expelled are so laughable and false.

Stanton said:

RotundOne said:

Evolutionary theory is critical in medicine and agriculture.

Well of course 98% of the theory is very useful and correct. But there are parts that have not been validated or do not really work out. These are the parts that many think should be looked at with a different point of view. Just as Newtonian physics explained 99% there still was a little that did not work. And if we do not allow criticism of the theory will never find out the whole story.

What aspects of Evolutionary Biology are wrong? Why is it that Creationists and Intelligent Design proponents are to be trusted to discover what this legendary 2% is, instead of the biologists who already study it? And while we're on the subject, please tell us why Creationists and Intelligent Design proponents are so keen to criticize Evolutionary Biology, but, have demonstrated that they have absolutely no desire to do or even understand science?

How can we falsify that basic tenet of the theory that natural selection is one of the largest mechanisms that causes random mutations to accumulate into different species and body plan changes? How do we know there is not another yet unknown mechanism causing all of this?

How can we falsify that basic tenet of the theory that natural selection is one of the largest mechanisms that causes random mutations to accumulate into different species and body plan changes? How do we know there is not another yet unknown mechanism causing all of this?

PvM said:

How can we falsify that basic tenet of the theory that natural selection is one of the largest mechanisms that causes random mutations to accumulate into different species and body plan changes? How do we know there is not another yet unknown mechanism causing all of this?

By hard work and showing that natural selection exists and that we can link mutations to differences in phenotype. As to whether or not there are other mechanisms, we already know of neutrality and there will undoubtably be room for others. However, ID does not provide us any answers to these questions really.

peter borger, biologist, PhD said: Ian, if you doubt the Schmid and Tautz (S&T) data on Drosophila in the PNAS, you should send them a letter. I did but they did not accept it (for obvious reasons). As you know (not?) S&T set up a screen for fast evolving genes, but they missed non-random mutations in the IG5 gene.

peter borger, biologist, PhD said: It is exactly what Truman and I showed for the indel on poistion 97 in Exon X of the GULO gene (you can get the article for free at the CMI if you ask).

But how can we falsify that NS is a mechanism? I do not see any studies doing that. That would be the first step.

With over 2,500 published estimates of selection gradients and differentials, our information about the strength of phenotypic selection in natural populations has expanded by more than fivefold since the time of Endler’s (1986) review.

PvM said:

But how can we falsify that NS is a mechanism? I do not see any studies doing that. That would be the first step.

John A. Endler "Natural Selection in the Wild" 1986 Princeton University Press ISBN:0691083878 Why did you assume that studies showing that NS is in fact a mechanism had not been done?

I am sure there are studies on it. But how can it be falsified? You understand falsification? Tell me: what would we observe if NS was not happening? Now common descent is easy: rabbits in the cambrian but NS is problem. This is my focus here.

How to falsify natural selection? Easy. If natural selection was falsified, then...

1. In a population of bacteria we would not see the emergence of resistance when exposed to antibiotics.

2. In a population of peppered moths we would not see dark moths come to predominate as the environment becomes more industrialised.

3. In a population of finches, we would not see beak anatomy change year by year as the weather (and thus the relative abundance of different types of nuts and other foods) changes.

There are, of course, many many other examples of empirical evidence that fits natural selection but could easily have falsified it if natural selection was not a real phenomenon. A quick Google search ought to dig up even more examples.

Tell me: what would we observe if NS was not happening?

RotundOne said: I am sure there are studies on it. But how can it be falsified? You understand falsification?

RotundOne said:

PvM said:

How can we falsify that basic tenet of the theory that natural selection is one of the largest mechanisms that causes random mutations to accumulate into different species and body plan changes? How do we know there is not another yet unknown mechanism causing all of this?

By hard work and showing that natural selection exists and that we can link mutations to differences in phenotype. As to whether or not there are other mechanisms, we already know of neutrality and there will undoubtably be room for others. However, ID does not provide us any answers to these questions really.

But how can we falsify that NS is a mechanism? I do not see any studies doing that. That would be the first step.

Got any improvement on that, other than bombast and the bathroom wall?

Voor Gerdien,

Leuk dat ik dan eindelijk de grote Gerdien de Jong tref. Het was toch alleen maar een kwestie van tijd. Ik lees nogal veel over en van je. Dat jullie het debat toch gaan winnen, enzovoort. Jammer dat ik er ook nog ben. En ik ben degene die het debat gaat winnen, niet jullie.

Tekenend voor het kamp waarin je zit is dat je hier beweert dat ik niet zou weten wat random betekent in de evolutionistiese betekenis. Het gebruikelijke verdraaien van feiten. Dat je het debat zo wilt willen (met leugens) verbaasd me niets, want je zit in het verkeerde kamp.

Zoals je had kunnen lezen, en waarschijnlijk ook wel hebt gedaan, heb ik bij Korthof, die mijn boek niet wilde bekritiseren omdat het het onomstotelijke einde betekent van het selectiemechanisme en van gemeenschappelijke afstamming, reeds uitgelegd wat jullie er onder verstaan en wat het in GUToB betekent, hoe je het kunt bepalen, dat het veel vaker voorkomt dan door de mainstreamers aangenomen. Samen met de beperkingen opgelegd door de functies van een eiwit (er zijn nogal wat functionele epitopen en complexiteits tioename is gewoon regulatie toename en dat vind je terug in de sequentie), geeft het een soort illusie, een genetiese mirage van gemeenschappelijke afstamming en hierarchiese clustering van soorten. Het bewijs wordt geleverd door de ad hoc hypotheses die jullie moeten invoeren om de hypothese, die reeds vele malen werd verworpen, te redden.

Jullie, Darwinisten, hebben de boel omgedraaid, ik draai het weer in de juiste richting. Mijn ideeen zijn gereed voor de 21ste eeuw.

Maar ik ben altijd bereid te luisteren en mijn boek moet nog krities worden gelezen. Misschien iets voor jou? Laat maar even weten.

Groet,
Peter

Voor Gerdien,

Leuk dat ik dan eindelijk de grote Gerdien de Jong tref. Het was toch alleen maar een kwestie van tijd. Ik lees nogal veel over en van je. Dat jullie het debat toch gaan winnen, enzovoort. Jammer dat ik er ook nog ben. En ik ben degene die het debat gaat winnen, niet jullie.

Tekenend voor het kamp waarin je zit is dat je hier beweert dat ik niet zou weten wat random betekent in de evolutionistiese betekenis. Het gebruikelijke verdraaien van feiten. Dat je het debat zo wilt willen (met leugens) verbaasd me niets, want je zit in het verkeerde kamp.

Zoals je had kunnen lezen, en waarschijnlijk ook wel hebt gedaan, heb ik bij Korthof, die mijn boek niet wilde bekritiseren omdat het het onomstotelijke einde betekent van het selectiemechanisme en van gemeenschappelijke afstamming, reeds uitgelegd wat jullie er onder verstaan en wat het in GUToB betekent, hoe je het kunt bepalen, dat het veel vaker voorkomt dan door de mainstreamers aangenomen. Samen met de beperkingen opgelegd door de functies van een eiwit (er zijn nogal wat functionele epitopen en complexiteits tioename is gewoon regulatie toename en dat vind je terug in de sequentie), geeft het een soort illusie, een genetiese mirage van gemeenschappelijke afstamming en hierarchiese clustering van soorten. Het bewijs wordt geleverd door de ad hoc hypotheses die jullie moeten invoeren om de hypothese, die reeds vele malen werd verworpen, te redden.

Jullie, Darwinisten, hebben de boel omgedraaid, ik draai het weer in de juiste richting. Mijn ideeen zijn gereed voor de 21ste eeuw.

Maar ik ben altijd bereid te luisteren en mijn boek moet nog krities worden gelezen. Misschien iets voor jou? Laat maar even weten.

Groet,
Peter

peter borger, biologist, PhD said: Voor Gerdien, Leuk dat ik dan eindelijk de grote Gerdien de Jong tref.

Ian says:

"No, that is not how it works. You have made a claim, you support it right here and now with evidence, not handwaving off to an article few can access. We have already done the heavy lifting here with regards to evidence. It is time for you to do some actual work and support your claims."

The silly thing is that you even show it in the above sequences. The position is an unstable position also in the other sequences. In primates it has become a deletion because the sequences and biochemistry are more similar. It may be related to repair mechanisms, integrated VIGEs, etc. Who knows? The nonrandom mechansim is nonrandom with respect to position and nuckleotide. If you had read my online ISCID paper (which is outdated now in its conclusions) you would have know what I mean with non-random mutations. They are not entirely stochastic.

Everybody knows that nowadays. It was known 5 years ago, when I discussed the topic at the EvC forum and was supported by Dr Caporale, who just released her book "Darwin in the genome".

But apparently nothing happened in evoland.

"Science commits suicide when it adopts a creed"

That's what you guys do.

An because nothing ever happens in evoland, I joined the other camp.

And I wrote my book.

"Because it [NS] has already been shown to be a mechanism decades ago."

Yep, read Edward Blyth. He wrote on it well before Darwin.

peter borger, biologist, PhD said: The silly thing is that you even show it in the above sequences. The position is an unstable position also in the other sequences.

In primates it has become a deletion because the sequences and biochemistry are more similar.

Ian says:

"It’s not their data that is at fault. It is your interpretation of it that is incorrect. Your only evidence for “non-random mutation” is your mistaken claim that Drosophila melanogaster is reproductively isolated, when in fact these fruit flies are constantly travelling around the world, hopping continents with gay abandon."

Wrong, Dr Musgrave, it is your interpreation that is incorrect.

It is clearly non-random mutations in the 1G5 gene. It was the fastest evolving gene. They simply missed this important observcation. I never miss important observations. If we would fail to notice significant things, science can't proceed.

For a science with a creed it is of course convenient to miss non-random mutations.

They're everywhere and I know how to determine.

"You are using the word “unstable” in a way not recognised by biologists."

That's why I had to write a book. With loads of novel jargon. To get rid of the obscuring screen Darwinians pulled over biology.

Some examples.

Homoplasy? It means: falsification of common descnet.

Endogenous retrovirus? It means variation inducing genetic element. The basis to understen the origin of viruses.

I was fed up with these obscurities, data selection, and incorrect interpretations.

"Now you are just making things up wholesale(even if it was “unstable” you have to posit an unparsimonious 4 independent deletion events in the primates to avoid common descent, you have no evidence for this)."

So what? The odds that HAR1F arose by chance are slimmer.

In particualr if position 97was a very unstable position and the primates went through a severe bottleneck. I remembered an old story and realized Noah's Arc explained.

by the way, if you eat fruit and herbs only, the GULO gene is an environment induced redundnat gene.

And that explains it all and that's why my new biology is ready to face the 21st century. I explain many observations that falsify Darwnin.

Ian Musgrave said:

peter borger, biologist, PhD said: Voor Gerdien, Leuk dat ik dan eindelijk de grote Gerdien de Jong tref.

Aber Leider, Neiderlandisch ist nicth unsere Muttersprache. Bitte Schreiben Sie auf Englisch.

RotundOne said:

PvM said:

But how can we falsify that NS is a mechanism? I do not see any studies doing that. That would be the first step.

John A. Endler "Natural Selection in the Wild" 1986 Princeton University Press ISBN:0691083878 Why did you assume that studies showing that NS is in fact a mechanism had not been done?

I am sure there are studies on it. But how can it be falsified? You understand falsification? Tell me: what would we observe if NS was not happening? Now common descent is easy: rabbits in the cambrian but NS is problem. This is my focus here.

It’s the same type of silly rant as all of it. Peter Borger is level UFO, as I remarked on the blog mentioned. It’s totally useless to argue with him.

— Gerdien de Jong

Evolutionary theory is critical in medicine and agriculture.

O, is it? What does it predict what I cannot predict without it?

How can I apply it to my field? Knocking out ADAM33 (a gene linked to bronchial hypperresponsive) in mice showed a no- phenotype knockout. Apparently the gene is redundant. That's what I expected. I predicted that upfront.

Six years ago I predicted the GULO exon X is subject to NRM. You can find my prediction on the EvC forum.

And indeed it is. Position 97 is a NR position.

Shared mutations in pseudogenes? NRM.

One more thing:

I do science, I never do ad hominem attacks.

I don't need ad hominem arguments, because I have science on my side. Not the scientists, that is, but science. The observable facts.

I know how we have to interpret the data.

You guys, including Professor De Jong, from the Uni of Utrecht, should address my scientifc comments.

The fact is you can't.

Because I have set up a better theory.

Get used to it.

Gerdien de Jong said:

RotundOne said:

PvM said:

But how can we falsify that NS is a mechanism? I do not see any studies doing that. That would be the first step.

John A. Endler "Natural Selection in the Wild" 1986 Princeton University Press ISBN:0691083878 Why did you assume that studies showing that NS is in fact a mechanism had not been done?

I am sure there are studies on it. But how can it be falsified? You understand falsification? Tell me: what would we observe if NS was not happening? Now common descent is easy: rabbits in the cambrian but NS is problem. This is my focus here.

In order to falsify natural selection one has to show that the covariance between phenotype and fitness always has to be zero. Any covariance other than zero between phenotype and fitness leads to a change in the phenotype, by simple algebra. Only if you show that the covariance between phenotype and fitness has to be zero in all cases can natural selection not exist. That is, when no trait is ever heritable - genetics does not exist; or when all individuals always have exactly the same number of offspring - variation does not exist. In other cases natural selection has to exist. And of course, natural selection has been shown to exist.

Somebody asked:

"How to falsify natural selection?"

Easy. Just knockout some genes, or ultraconserved regions in mice, and if they don't give a phenotype...

...you may ask yourself how on earth could these sequences survive the ages.

And that is what you can read about next months in J. Creat. I personally wrote it for you. Free evology from Darwin and start thinking again. I did that seven years ago and I am far ahead of you. I undertstand all biology.

Natural selection has been falsified beyond any doubt. It is of NO relevance in explaining the content of genomes.

The issue is: you don't believe it.

"The toolkit wasn’t built up over time, courtesy of NS. That is a published, observed fact."

Exactly my point. Science shows genomes were frontloaded with an excess of genetic elements (that still show up as genetic redundancy in knockout stratagies) and had a built-in mechanism for rapid changes. The evolution we observe is alwyay fast isn't it? How come? Because the variation is induced from inside by variation inducing genetic elements (mainstreamers know them as ERVs, LINEs, SINEs, ALU, transposons, and the like). Multipurpose genomes were designed as baranomes in order to rapidly adapt. Sometimes natural slection plays a role, but it is not a relevant or major evolutionary force.

My review to provide the molecualr evidence for baranomes, and how they work, will appear in September or so.

You will call me a crank, but I don't mind.

I am right, that is all that matters.

peter borger, biologist, PhD said: Somebody asked: "How to falsify natural selection?" Easy. Just knockout some genes, or ultraconserved regions in mice, and if they don't give a phenotype... ...you may ask yourself how on earth could these sequences survive the ages. And that is what you can read about next months in J. Creat. I personally wrote it for you. Free evology from Darwin and start thinking again. I did that seven years ago and I am far ahead of you. I undertstand all biology. Natural selection has been falsified beyond any doubt. It is of NO relevance in explaining the content of genomes. The issue is: you don't believe it.

Professor de Jong, ik maak ook wel even een Volkskrantblog, want ik houd niet van ad hominem argumenteren. En zeker niet op deze manier. Als u commentaar heeft doe dat dan op een wetenschappelijke manier. Ik copy en paste wel even wat.

Ik noem het: "Professor de Jong's UFO level"

U bent van harte uitgenodigd op mijn blog om mijn ideeen wetenschappelijke te weerleggen.

RotundOne said: I guess I was not specific enough: How can we falsify that NS leads to speciation and major body plan changes?

"So if NS selection does not work how did all the species and body plans come to be?"

Not by natural selection, my friend. NS is the phlogiston of current evology.

The informtation in the baranomes was frontloaded, probably ex nihilo and in excess, by someone. And as far as I can judge this someone was pretty intelligent and foreseeing. I call this someone the great omnipotent designer (G.O.D).

peter borger, biologist, PhD said: "So if NS selection does not work how did all the species and body plans come to be?" Not by natural selection, my friend. NS is the phlogiston of current evology. The informtation in the baranomes was frontloaded, probably ex nihilo and in excess, by someone. And as far as I can judge this someone was pretty intelligent and foreseeing. I call this someone the great omnipotent designer (G.O.D).

"A ‘toolkit’ once present can be used again."

Not without selection, dear prof.

Read a bit into genetic redundancy. You will find 1) redundant genes are not associated with gene duplications, 2) do not mutate faster than essential genes, 3) can not reside in genomes for ages because NS doesn't act on them.

That overturns 1)Ohno, 2) Kimura,3) Darwin. That's a lot, isn't it.

You are free to ignore this.

Because I have set up a better theory.

— peter borger

That overturns 1)Ohno, 2) Kimura,3) Darwin. That’s a lot, isn’t it.

Gerdien de Jong says: “Only if you show that the covariance between phenotype and fitness has to be zero in all cases can natural selection not exist. That is, when no trait is ever heritable - genetics does not exist; or when all individuals always have exactly the same number of offspring - variation does not exist. In other cases natural selection has to exist. And of course, natural selection has been shown to exist.”

.

Indeed, any way you cut it, NS is a truism, since fitness is essentially defined by survival. It simply has to be true, at least in this particular universe of the multiverse. Additionally NS does have predictive power, roughly akin to the predictive power of weather forecasting.

peter borger, biologist, PhD said: In particualr if position 97was a very unstable position

and the primates went through a severe bottleneck. I remembered an old story and realized Noah's Arc explained.

peter borger, biologist, PhD said: It is clearly non-random mutations in the 1G5 gene. It was the fastest evolving gene.

Better than Behe’s “theory”?

What is his theory?

"Just being a fast evolving gene does not make something non-random. Your only evidence that this gene is evolving randomly was the geographic distribution. Unfortunately for you, Drosophila melanogaster is not reproductively isolated, and hops around the world quite rapidly that Preu and America share the same genotype is due to invasion, not non-random mutation."

I said this was the FIRST evidence I encountered that made me think about the true character of mutatiosn. First evidnce. Currently, there is plenty of evidence for NRM. I even know WHEN (the trigger) a particular type of NRM are introduced in sequences.

For your assertion: proof it. Show a genetic marker that proofs the invasion of American species in Peru. Or Autralian species in N-America. Or vice versa.

If you don't it is just another just so story to keep up an appearance.

Even the ancient human mtDNA show NRM. Scott Page can tell you all about it? I pointed it out for him in an EvC debate, just before he got banned in 2003. Did he never mention?

Did Ancient humans hop around in airplanes? Probably. In evology everything is possible.

Even the ancient human mtDNA show NRM. Scott Page can tell you all about it? I pointed it out for him in an EvC debate, just before he got banned in 2003. Did he never mention?

Did Ancient humans hop around in airplanes? Probably. In evology everything is possible.

Trolls have been moved to the Bathroom Wall.

RotundOne said:

Stanton said:

RotundOne said:

Evolutionary theory is critical in medicine and agriculture.

Well of course 98% of the theory is very useful and correct. But there are parts that have not been validated or do not really work out. These are the parts that many think should be looked at with a different point of view. Just as Newtonian physics explained 99% there still was a little that did not work. And if we do not allow criticism of the theory will never find out the whole story.

What aspects of Evolutionary Biology are wrong? Why is it that Creationists and Intelligent Design proponents are to be trusted to discover what this legendary 2% is, instead of the biologists who already study it? And while we're on the subject, please tell us why Creationists and Intelligent Design proponents are so keen to criticize Evolutionary Biology, but, have demonstrated that they have absolutely no desire to do or even understand science?

Well for instance some of the validation for the theory seems to be weak. And we should really go into those weak areas and look around a bit.

peter borger, biologist, PhD said: I said this was the FIRST evidence I encountered that made me think about the true character of mutatiosn. First evidnce.

Gerdien de Jong said:

Ian Musgrave said:

peter borger, biologist, PhD said: Voor Gerdien, Leuk dat ik dan eindelijk de grote Gerdien de Jong tref.

Aber Leider, Neiderlandisch ist nicth unsere Muttersprache. Bitte Schreiben Sie auf Englisch.

Neiderlandisch is a good mistype for Niederlaendisch, as it makes the connection to 'Neid', = wrath, jealousy. It's the same type of silly rant as all of it. Peter Borger is level UFO, as I remarked on the blog mentioned. It's totally useless to argue with him.

Position 97 is no more “unstable” than many other positions in the GULO gene, like positions 49 and 85 for example (hint, rat and mouse sharing a mutation does not mean the position is unstable).

rat and mouse descended from one baranome.

97 is a NR position. We find a different nucleotide on this position in all other animals. In humans and primates, because of their biochemistry and sequences are more similar (almost the same), the unstable position becomes manifest as an indel. Give me one valid reason why it wouldn't?

Would someone be kind enough to tell me how to get to the bathroom wall, so I can go on having a conversation? Thankyou. Regards. P.H.

"And now that your supposition has been shown to be wrong, what do you think? This wasn’t evidence, but your ignorance, it is well known Drosophila melanogaster moves around the world (the Australian Quarantine service is on the look out to prevent new invasions of this fly)."

If you were setting up a screen for fast-evolving genes, what would you do?
Exactly.

Schmid and Tautz deliberately took endemic populations. Your explanation can be excluded.

Some theories such as natural selection are so well validated that it is hard to falsify them these days. Which is what the National Academy of Sciences said in their recent statement on evolution.

We forget that it wasn't always that way. When Darwin proposed his explanation, in 1860, even he wasn't all that sure. In the 150 years since, RM + NS has been attacked unmercifully by other scientists and religious fanatics, modified, and extended. It has withstood all assaults to the point where some religious fanatics have given up beating up on the theory and started beating up on scientists instead.

Some other theories show a similar property.

1. The theory of neutron mediated fission of a few heavy elements. Such as uranium 235 and plutonium. To falsify this, all power reactors in the world should stop running, the lights should go out, and a few cities in Japan should have a different downtown.

2. The germ theory of disease. I suppose if this was falsified, no one would die of malaria, HIV, TB, MRSA, or get sick with the flu.

RM + NS won in the arenas of science and educated people 75 years ago and they moved on. These days it is attacked almost exclusively by religious fanatics with an agenda.

peter borger, biologist, PhD said: 97 is a NR position. We find a different nucleotide on this position in all other animals. In humans and primates, because of their biochemistry and sequences are more similar (almost the same), the unstable position becomes manifest as an indel. Give me one valid reason why it wouldn't?

peter borger, biologist, PhD said: Schmid and Tautz deliberately took endemic populations. Your explanation can be excluded.

Eh, Raven, if natural selection and survival of the fittest was true, no one would, indeed, "die of malaria". You're RM + NS has successfully manufactured tens of thousands of resilient species, survived two massive extinction events, brought us instant stirfry and even indoor plumbing - courtesy of creating Man - so naturally selecting us so we don't get malaria, would be a breeze. But why didn't it give us fur, to keep us warm at night? Did great-great grandaddy microbe select wrongly back there or something?

Eh tell us something I haven't heard 50 times before and explain accessing the Bathroom Wall, please.

PBH - here's your answer:
http://www.antievolution.org/cgi-bin/ikonboard/ikonboard.cgi?s=483d6d6f495a8f58;act=ST;f=14;t=1272;st=6510

Someone wrote:

"1) gene duplications happen, this has been observed fairly often, and the result is redundant genes; "

PB: This is not in doubt. It is an important observation and it is fact.

"2) Redundant genes have more freedom to mutate in the sense that the organism is more likely to survive mutations in redundant genes (which are more likely to be nearly neutral);"

PB: This is Ohno's story. It is a nice story but doesn't work. See my papers with Truman in J Creat, last month and last year (do a google and you will find them).
fact is there is no association with duplications. So, we have independent arrivals of genes with the same or similar function without natural selection to shape them. Moreover, redundant genes do not accumulate more mutations than essential genes. Ohno predicted 10 pseudogenes to every novel gene (where did he get these numbers from anyway; just a guess would be my guess). The 10:1 pseudogenes are not in the genome. It is the other way around: in the genomes we see the birth of about 2000 novelties and the death of about 200. That is fact. If you wish I can give you the exact figures.

"3) Redundant genes have a time limit within which they should become involved in something useful, otherwise they may devolve into the “junk dna” category. Even so, bits and pieces may someday be resuscitated and put to some unexpected purpose."

This is a presupposition, but the observations can be interpreted the other way around, easily. Like the cited Cai & Zhao paper. That two genes merge to form one? So be it. When two join to become one you must first explain the existence of two, then I explain the existence of one. Easy.

You need to posit an unknown enzyme, that for unknown reasons, deleted the same site independently 4 times.

No, I don't. Every hematologist can tell you that breaks and translocations causing leukemia are usually found in the exact same location in the genes.

It's damage-repair mediated. Some are mediated by transposable elements.

"No, they just took the available local populations."

Endemic populations. Why did they do that, do you think? To set up a screen for fast evolving genes. How would you set that up? By taking just local populations? That would be bad science. They took endemic populations from all over the world and it showed NRM (although they missed the observation).

The ancient mtDNA also show this phenomenon. Ask Scott Page. He is also lurking around somehwere and he knows since 2003. I told him.

"Some theories such as natural selection are so well validated that it is hard to falsify them these days. Which is what the National Academy of Sciences said in their recent statement on evolution."

Apparently they never heard about genetic redundancy.

bigbang said: Gerdien de Jong says: “Only if you show that the covariance between phenotype and fitness has to be zero in all cases can natural selection not exist. That is, when no trait is ever heritable - genetics does not exist; or when all individuals always have exactly the same number of offspring - variation does not exist. In other cases natural selection has to exist. And of course, natural selection has been shown to exist.” . Indeed, any way you cut it, NS is a truism, since fitness is essentially defined by survival. It simply has to be true, at least in this particular universe of the multiverse. Additionally NS does have predictive power, roughly akin to the predictive power of weather forecasting.

" Some theories such as natural selection are so well validated that it is hard to falsify them these days. "

I cannot believe they said that. A good theory must be falsifiable.

Are you sure you got the quote correct?

I cannot believe they said that. A good theory must be falsifiable. Are you sure you got the quote correct?

RotundOne said: " Some theories such as natural selection are so well validated that it is hard to falsify them these days. " I cannot believe they said that. A good theory must be falsifiable. Are you sure you got the quote correct?

peter borger, biologist, PhD said: "You are using the word “unstable” in a way not recognised by biologists." That's why I had to write a book. With loads of novel jargon. To get rid of the obscuring screen Darwinians pulled over biology.

Flint said:

I cannot believe they said that. A good theory must be falsifiable. Are you sure you got the quote correct?

You have missed the extremely subtle distinction between a theory being falsifiable, and a theory being false. Imagine, just for a moment, a theory which just happens to be correct. Can it be falsified? Not very easily!

Which is why they have such a severe phobia of evidence.

As I understand it, the basic question for falsifiability is “If you were wrong, how would you know?”

Gerdien de Jong says: “Anything that involves algebra is a truism in some sense….”

.

No, not really. You’re confusing “equal to” with “is defined by.” e=mc^2, or 1+1=2; but fitness "is defined by" survival (and obviously reproduction).

bigbang said: Gerdien de Jong says: “Anything that involves algebra is a truism in some sense….” . No, not really. You’re confusing “equal to” with “is defined by.” e=mc^2, or 1+1=2; but fitness "is defined by" survival (and obviously reproduction).

The Revenge of the Serpent

From http://www.sciencedaily.com/releases/2008/05/080520203007.htm----

.

“ScienceDaily (May 23, 2008)----Prior to the advent of large sequence datasets, it was assumed that innovation and divergence at the morphological and physiological level would be easily explained at the molecular level. Molecular explanations for physiological adaptations have, however, been rare. Pollock and colleagues now provide evidence that major macroevolutionary changes in snakes (e.g., physiological and metabolic adaptations and venom evolution) have been accompanied by massive functional redesign of core metabolic proteins.”

.

A massive functional redesign----to some, more proof of the fact and power of evolution by RM+NS. To others, more evidence indicating the edge of evolution via RM+NS.

peter borger, biologist, PhD said: No, I don't. Every hematologist can tell you that breaks and translocations causing leukemia are usually found in the exact same location in the genes.

A massive functional redesign—-to some, more proof of the fact and power of evolution by RM+NS. To others, more evidence indicating the edge of evolution via RM+NS.

peter borger, biologist, PhD said: They took endemic populations from all over the world and it showed NRM (although they missed the observation).

peter borger, biologist, PhD said: "Some theories such as natural selection are so well validated that it is hard to falsify them these days. Which is what the National Academy of Sciences said in their recent statement on evolution." Apparently they never heard about genetic redundancy.

RotundOne said: " Some theories such as natural selection are so well validated that it is hard to falsify them these days. " I cannot believe they said that. A good theory must be falsifiable. Are you sure you got the quote correct?

PvM said:

A massive functional redesign—-to some, more proof of the fact and power of evolution by RM+NS. To others, more evidence indicating the edge of evolution via RM+NS.

And those 'others' lack any explanations

peter borger, biologist, PhD said: No, I don’t. Every hematologist can tell you that breaks and translocations causing leukemia are usually found in the exact same location in the genes.

1: Leuk Res. 2008 Apr;32(4):579-85. Epub 2007 Oct 24. Links A multiplex PCR for improved detection of typical and atypical BCR-ABL fusion transcripts.Burmeister T, Reinhardt R. Charité Universitätsmedizin Berlin, Campus Benjamin Franklin, Medizinische Klinik III, Hindenburgdamm 30, 12200 Berlin, Germany. RT-PCR is the method of choice for detecting BCR-ABL in CML and ALL. The three predominant mRNA transcripts found are e1a2 (in ALL), e13a2, and e14a2 (in CML and ALL). However, a number of "atypical"BCR-ABL transcripts (e1a3, e13a3, e14a3, e19a2, e6a2, e8a2, etc.) resulting from chromosomal breakpoints outside ABL intron 1 or BCR intron 1, 13 or 14, respectively, have been reported. These atypical transcripts may escape detection when using methods that are optimized to detect just the typical ones. We present here a novel, fast, and reliable multiplex PCR for improved detection of typical and atypical BCR-ABL transcripts.

PvM says: “And those ‘others’ lack any explanations”

.

Well, there’s always Koonin’s infinite multiverse.

From Einstein’s general relativity equations (and other evidence) Lemaitre, a Catholic priest and physicist, determined that the universe seemed to be expanding, and in 1931 suggested that the expansion in forward time required that the universe contracted backwards in time, bringing all the mass of the universe into a single point, a primeval atom, at a point in time before which time and space did not exist.

Hoyle found the idea of the universe having a beginning to be philosophically troubling (being an atheist at the time), and along with many others argued that a beginning implies a cause, a creator, and derisively referred to Lamaitre’s idea as his big bang idea. (Hoyle later rejected his atheism.)

Fast forward to today----From actual evolutionary data and other evidence, Behe, a Catholic and microbiologist, determines that there is a limit to what evolution by RM+NS can actually accomplish, and that much of the complexity of life implies design rather than the unintelligent, undirected process of RM+NS; but neo-Darwinians find Behe’s idea to be philosophically troubling (most neo-Darwinians being atheists), arguing that design implies God, and they refer to Behe and his insight in all sorts of disparaging ways.

So what’s new? From Galileo on there have always been those that see beyond whatever establishment groupthink happened to be in place at the time.

From Galileo on there have always been those that see beyond whatever establishment groupthink happened to be in place at the time.

bigbangBigot, you refuse to realize that all of the alleged "limits" to evolution and Random Mutation + Natural Selection have been proven false. Behe never performed any experiments to test the alleged "limits," and all of his criticisms of evolutionary processes have been torn apart on this blog, on other blogs, and in print, repeatedly. All of Behe's arguments have been revealed to be nothing more than fancifully worded arguments from his own incredulty, made especially painful because he refuses to acknowledge contrary evidence, and that he refuses to acknowledge his critics, save to insult them like he did with ERV.

In other words, bigbangBigot, in order to claim that Behe is another Galileo, he has to have been right, which he is not.

bigbang said: ...but neo-Darwinians find Behe’s idea to be philosophically troubling (most neo-Darwinians being atheists), arguing that design implies God, and they refer to Behe and his insight in all sorts of disparaging ways.

bigbang said: PvM says: “And those ‘others’ lack any explanations” Well, there’s always Koonin’s infinite multiverse.

Fast forward to today----From actual evolutionary data and other evidence, Behe, a Catholic and microbiologist, determines that there is a limit to what evolution by RM+NS can actually accomplish, and that much of the complexity of life implies design rather than the unintelligent, undirected process of RM+NS; but neo-Darwinians find Behe’s idea to be philosophically troubling (most neo-Darwinians being atheists), arguing that design implies God, and they refer to Behe and his insight in all sorts of disparaging ways.

So what’s new? From Galileo on there have always been those that see beyond whatever establishment groupthink happened to be in place at the time.

Behe, a Catholic and microbiologist

Dang, forgot to mention that Behe used to be a biochemist, NOT a microbiologist. He only plays one when he's not on witness stands.

Flint sez... This may or may not be a semantic quibble, but I’ve yet to see any good indication that creationists really understand what evidence means. The closest I’ve seen any of them come is, speculations ... that support their foregone conclusions are “evidence”.

PvM said: Genetic degeneracy... Small difference but big in its extent. In fact, natural selection is part of the explanations for the origin and evolution of the genetic code. In fact, the degeneracy of the genetic code may not just be an important reason for the success of evolutionary processes (evolvability) but it should also be realized that such neutrality can in fact be under selective pressures. Just because the genetic code evolved in manners that involved other processes than just natural selection does not mean that NS was falsified, on the contrary.

peter borger, biologist, PhD said: "Some theories such as natural selection are so well validated that it is hard to falsify them these days. Which is what the National Academy of Sciences said in their recent statement on evolution." Apparently they never heard about genetic redundancy.

Ian, why are you unable to discuss the topic without being condescending? Is it so hard to keep up the paradigm?

I used to work in the hematology lab where most of my colleagus studied AMLs. The finding was that translocations were in 80% on exactly the same spot. I've seen the data, they've been published and it made me think about the true nature of how mutations might be introduced: non-stochastic. That is about 13 years ago, when I still was a PhD student. I have had a long way to think about the matter. When everybody was setting up new ad hoc hypothesis to explain away the data that falsify Darwin, my midn already wopkde on a novel theory. Now, a decade later I know how to determine what part of mutaions is non-random. I know several mechanism that give an illusion of common descnet. I will present them in my forthcoming book. That will be the end of the Darwinian era.

How do we discriminate between a super hot spot that changed in the past in several species independently and a position you take as evidence for common descent? Position 97 might be such position. Because of HAR1F and other Darwin CD falsifying observations I take it as a NRM; A super hotspot that fixed independently in primates because of a severe bottleneck.

Ian,
Regarding the Drosophila paper (I thought you said I had to stay on topic: GULO).

Anyway,

In this paper, Karl J. Schmid and Diethard Tautz, two biologists of the University of Cologne discussed fast evolving genes in Drosophila melanogaster and Drosophila simulans. The focus was on the 1G5 gene. This gene is found in both species as a unique single copy gene; it is of unknown function but not an inactive pseudogene. The 1G5 gene had the authors’ particular interest because it was the fastest changing gene of their study. From protein coding part of the 1G5 gene counts 1’081 base pairs, which includes only one small intron of 61 base pairs. Schmid and Tautz located all mutations in an 864 base pair segment, which included the intron, in thirteen populations of D. melanogaster and four of D. simulans. It turned out that the major part of the individual genes is identical and not interesting for analysis. Only a handful of mutations was observed between the subpopulations of fruit flies a few dozens between the two species. Most of them are point mutations, but there are also indel mutations of more than one nucleotide in this part of the gene. The left side of figure 16-1 shows the mutations observed in the 61 base pair intron; the right hand side shows the mutations in the 803 base pair fragment of the coding region (exon 2). The numbers 141 to 922 at the top of the figure indicate the exact location of the mutations present in the 1G5 gene. It shows that the fraction of variable sites in the non-coding part (the intron) and the protein-coding part (the exon) of the 1G5 gene is approximately the same. The authors concluded that:

Almost none of the amino acid positions may be under strong selective constraint, because the fraction of polymorphic sites in the intron is comparable to the fraction of polymorphic sites in the coding region. […] Comparison between fixed and polymorphic sites between the two species shows also no significant deviation from the assumption of a neutral evolution in this region.

Is that all – neutral evolution in this region? Is there nothing more to say about the 1G5 genes? As a matter of fact the genes demonstrate some very intriguing phenomena that went unnoticed by the authors.

Let’s have a look at the figure they present (you have the article in front of you so look at it carfully).

The introns of the individual genes vary considerably between the two distinct species (13 out of 61 nucleotides are different: 21%), introns within subpopulations of D. melanogaster show nearly no variation (1 out of 61 nucleotides vary in only 3 out of 13 subpopulations: 1.6%). Similarly, introns in the 1G5 gene found in the subpopulations of D. simulans do not demonstrate variation at all. This is peculiar, since it is expected that the highest incidence of mutations is within the intron regions of a gene. The neutral theory tacitly assumes that introns are not subject to selection and accumulate mutations at random. This is not only expected in reproductively isolated species, but also between isolated subpopulations of one species. Yet, we do not see variation within the introns of subpopulations. A careful look at the positions of the mutations in the introns between the species shows the intron accumulated thirteen mutations of which ten are immediately adjacent to each other (numbers 153-162). The chance that ten point mutations occur at random in the intron equals 1.4 x 10-18. By way of contrast, the chance that ten adjacent mutations occur in the intron equals 2.2 x 10-14. Natural selection can’t explain this cluster of mutations. Introns are assumed to be evolutionary neutral, in that selection does not act on them. If you want to invoke Darwin's magic word to explain the fixed cluster, it must have arisen by selection on neutral positions. That is neutral selection. It is therefore reasonable to assume that the cluster of mutations observed in the introns is not the result of chance.

Another remarkable observation is that the 1G5 genes in subpopulations of D. melanogaster, as far apart as Australia, Russia or Canada are completely identical. It implicates a very high level of stability of the DNA sequences within species. Even within the highly unstable 1G5 gene. Evolutionists may speculate that these identical populations were derived from a common founder population that repopulated the area after an ice age, or so. But, why would an Australian and not a Japanese or Mexican population of D. melanogaster - which would make much more sense - take over the empty niches in Russia and Canada? And even if it happened like that, it would not explain the observation of the invariable fixed intron in the 1G5 gene of D. simulans. Neither would it explain the cluster of 10 adjacent mutations in the introns of both species.

There is even more. A careful comparison of exon2 of the 1G5 gene of both Drosophila species uncovers that the genes change with distinctly different rates. Subpopulations of D. melanogaster demonstrate an average of nearly 3 mutations of 803 possible locations (0.37%), whereas subpopulations of D. simulans exhibit and average of 14 mutations (1.7%). Moreover, D. simulans, but not D. melanogaster, demonstrates insertion-deletion mutations in the 1G5 gene.
Clearly, the genes change at different rates and suggest that the genes have distinct functions in either organism.

The sequences of the three Australian subspecies could't descent from other without invoking NRM. Try it, and tell me how, if it is possible.

The data provided by Schmidt and Tautz showed that natural selection was unlikely to act on the 1G5 gene. The consequence is that the shared mutation in the 1G5 genes must be due to a biological or physical mechanism .

I discussed this years ago.

Scott Page commented then: A fluke.

Your comments now: migration.

What is it? NRM.

Ciao,
Peter

Next, we can go through the ancient human mtDNA. I will again proof my point of NRM, Scott Page will jump in telling I am a moron, a fool, or whatever, and then in five years or so, I will do it again on another board.

History is repeating itself and nothing is going on in evoland.

Sleep well.

Peter

peter borger, biologist, PhD said: In this paper, Karl J. Schmid and Diethard Tautz, two biologists of the University of Cologne discussed fast evolving genes in Drosophila melanogaster and Drosophila simulans.

Let’s have a look at the figure they present (you have the article in front of you so look at it carfully).

The introns of the individual genes vary considerably between the two distinct species (13 out of 61 nucleotides are different: 21%), introns within subpopulations of D. melanogaster show nearly no variation (1 out of 61 nucleotides vary in only 3 out of 13 subpopulations: 1.6%). Similarly, introns in the 1G5 gene found in the subpopulations of D. simulans do not demonstrate variation at all. This is peculiar, since it is expected that the highest incidence of mutations is within the intron regions of a gene.

A careful look at the positions of the mutations in the introns between the species shows the intron accumulated thirteen mutations of which ten are immediately adjacent to each other (numbers 153-162).

Another remarkable observation is that the 1G5 genes in subpopulations of D. melanogaster, as far apart as Australia, Russia or Canada are completely identical. It implicates a very high level of stability of the DNA sequences within species. Even within the highly unstable 1G5 gene. Evolutionists may speculate that these identical populations were derived from a common founder population that repopulated the area after an ice age, or so. But, why would an Australian and not a Japanese or Mexican population of D. melanogaster - which would make much more sense - take over the empty niches in Russia and Canada? And even if it happened like that, it would not explain the observation of the invariable fixed intron in the 1G5 gene of D. simulans. Neither would it explain the cluster of 10 adjacent mutations in the introns of both species.

That backs up the HOX genes - paddlefish story and is as near to proof that anyone needs, that something far more sophisticated than mere NS was involved in evolution.

Ian Musgrave said: There were no populations of D. melanogaster in Canada (or the rest of the American continent) before around 130 years ago, and none in Australia before the 1900's. All the D. melanogaster in the Americas and Australasian area are invaders. They mostly derive from Eurasian populations (which are pretty homogeneous), although there are a small proportion that derive from African populations. An Australian population could not take over a Russian niche as there was no Australian population (or Japanese or Mexican population as there was no Drosophila in Japan before the 1960's, and none in Mexico before around the 1900's). Drosophila evolved in Africa, then invaded Eurasia. Humans then took Drosophila to the Americas and Australasia in their ships.

Eurasian and African Drosophila populations have entered the Americas and Australasia multiple times since the first colonization events. Here your analysis fails as you are ignorant of organsimal biology.

PBH rants .... Then there are ant-creationists who send articles out of NATURE, and SCIENCE, and such like, to the bathroom wall - ONLY IF THE ARTICLE DOESN’T SUIT THEIR POINT OF VIEW. Then they sit on the white throne of “science”, and say that everyone else is ignorant.

Flint said:

That backs up the HOX genes - paddlefish story and is as near to proof that anyone needs, that something far more sophisticated than mere NS was involved in evolution.

I fail to follow this reasoning. Imagine that a DNA test indicates that a child's father is someone other than his mother's husband. This happens from time to time. Does this constitute "as near to proof that anyone needs" that human breeding doesn't work the way we think it does? That something "far more sophisticated" is involved?

Flint said: What you've pointed out is a suggested change in the previously proposed clade diagram, which has nothing to do with the mechanisms by which clades evolve. So now a new diagram is proposed? OK, what's the problem?

"The foundation of Creationism is always ignorance"

Was I talking about creationism? No, I was talking about Non-random mutations. Because you can't show how the populations werde derived from each other in a diagram, it leaves us with the only option of non-random mutations in the 1G5 genes to explain the alignment of several mutations.

If not, show how they evolved. Scott page couldnt, I can't, and you cannot.

We can't, because the mutations are not introduced at random.

Goodbey, Darwinism.

Ian, continues his condescending style:

"The foundation of Creationism is always ignorance"

I wasn't talking about creationism, I was talking about non-random mutations. Whether or not the indel shifted or got lost is not relevant to observe the NRM in D. mel. I thought you were going to respond to that?

Because you can't show how the D. mel populations were derived from each other, the nmigration and evolution pattern, it leaves us with no other option of non-random mutations in the 1G5 genes in D. mel. to explain the alignment of several mutations.

If not, show how they migrated and evolved.

If it can't be done, the mutations are introduced in a non-random fashion.

peter borger, biologist, PhD said: Ian, I was talking about non-random mutations in D mel's 1G5 gene. Whether or not the indel shifted or got lost is not relevant to observe the NRM in D. mel. I thought you were going to respond to that? Because you can't show how the D. mel populations were derived from each other, the nmigration and evolution pattern, it leaves us with no other option of non-random mutations in the 1G5 genes in D. mel. to explain the alignment of several mutations. If not, show how they migrated and evolved. If it can't be done, the mutations are introduced in a non-random fashion.

The revenge of the Drosphila:

Ian says, and I agree:

"There were no populations of D. melanogaster in Canada (or the rest of the American continent) before around 130 years ago, and none in Australia before the 1900’s. All the D. melanogaster in the Americas and Australasian area are invaders. They mostly derive from Eurasian populations (which are pretty homogeneous), although there are a small proportion that derive from African populations.
An Australian population could not take over a Russian niche as there was no Australian population (or Japanese or Mexican population as there was no Drosophila in Japan before the 1960’s, and none in Mexico before around the 1900’s). Drosophila evolved in Africa, then invaded Eurasia. Humans then took Drosophila to the Americas and Australasia in their ships. Eurasian and African Drosophila populations have entered the Americas and Australasia multiple times since the first colonization events."

The sequences show:

An Italian population invaded the Americas, first the USA (D. mel III) and then it migrated to Peru. In Peru this population acquired the exact same mutation as, and independent of, the population in Japan (the A at position 835).

A population of Cyprus, Irak or USSR invaded Canada and USA (USA II). The populations in Australia were not derived from the Italian. Still, the Australian population ends up with the exact same mutation the Italian population acquired in the USA (The C at position 498).

The Australian population (D. mel 3) could have migrated from the USA (D mel 11), and acquired an A at position 637.

Conclusion:

1) mutation rates are high,

2) mutations are not merely introduced at random.

peter borger, biologist, PhD said: Ian, I was talking about non-random mutations in D mel's 1G5 gene. Whether or not the indel shifted or got lost is not relevant to observe the NRM in D. mel. I thought you were going to respond to that?

Because you can't show how the D. mel populations were derived from each other, the nmigration and evolution pattern, it leaves us with no other option of non-random mutations in the 1G5 genes in D. mel. to explain the alignment of several mutations. If not, show how they migrated and evolved. If it can't be done, the mutations are introduced in a non-random fashion.

Not that this comment thread hasn't been fun, but I have to prepare for the Australian Society Medical Research congress and read my students final PhD Thesis draft. As I won't be able to monitor the thread, and to stop trolls taking over, I'm going to turn off comments.

People who wnat to follow up Trolls on the bathroom wall, go here