!	MODNOTE Split interesting topic into its own thread. Durro

To play the devil's advocate for a second, I just noticed that Michael Behe has brought out a serious paper:-

http://www.lehigh.edu/~inbios/pdf/Behe/QRB_paper.pdf

I have not had time to read it properly yet, but it does not look too bad.

Commentary on Panda's Thumb suggests he's made some good observations, and found some good places to suggest further scientific inquiry is warranted, but that he's then gone on within the ID community to trumpet unpublished "conclusions" which simply aren't supported by the paper or by reality.

http://pandasthumb.org/archives/2010/12 ... l#comments

PT's Ichythic wrote:(M)aybe he should have spent the last five years reading those 50+ books and journal articles that he admited to never having read…

strangely enough, it looks like he has finally gotten that message.

did you read his last published paper?

no, I didn’t either, but evidently while some of his conclusions, of course, are entirely delusional, people involved with microbial genetics and evolution feel he was indeed spot on in calling for more research looking into the evolution of novel traits.

http://whyevolutionistrue.wordpress[…]ies-to-behe/

so, this time at least, Behe DID take the time out to peruse the lit, DID notice some areas that needed more research, and only then tried to stuff his god into those gaps.

Is that progress?

maybe he’s trying to actually get interested in doing real science again.

We’ll see if his religious delusions keep getting in the way.

And the review of the MB paper he cited:
http://whyevolutionistrue.wordpress.com ... s-to-behe/

Which includes the following:

Behe’s implicit conclusion was that evolution in nature—and not just in bacteria and viruses, but all species—also occurred in this way; that is, brand-new genes or genetic elements (he calls them “FCTs”) could not originate de novo by mutation and natural selection, but had to be put there by the Intelligent Designer (aka God/Jebus). Behe did not, and could not, say this in the paper, but intelligent-design advocates certainly touted this conclusion (see here and here, for instance), and now Behe himself has said the same thing on his blog at Uncommon Descent:

Behe wrote:. . . I was saying that, no matter what causes gain-of-FCT events to sporadically arise in nature (and I of course think the more complex ones likely resulted from deliberate intelligent design http://tinyurl.com/32n64xl), short-term Darwinian evolution will be dominated by loss-of-FCT, which is itself an important, basic fact about the tempo of evolution.

Note that here he doesn‘t limit this conclusion (which he conveniently omitted from the QRB paper) to bacteria and viruses.

Weaver wrote:
And the review of the MB paper he cited:
http://whyevolutionistrue.wordpress.com ... s-to-behe/

Which includes the following:

Behe’s implicit conclusion was that evolution in nature—and not just in bacteria and viruses, but all species—also occurred in this way; that is, brand-new genes or genetic elements (he calls them “FCTs”) could not originate de novo by mutation and natural selection, but had to be put there by the Intelligent Designer (aka God/Jebus).

Which is actually a testable hypothesis. Not the Designer/Jebus/God part, but the claim that "new genes" cannot arise thru evolutionary processes. Or, even less stringently, that "new genes" exist that cannot be related to evolutionary precursors, which is not quite the same thing. One way the IDers could have supported this position was suggested in this video:

[youtube]http://www.youtube.com/watch?v=ZkED8cWRu4Q[/youtube]

The closest thing to a response from the DI I could find is this. Predictably, they don't actually acknowledge that they cannot answer the challenge, but instead just come up with excuses and non-sequitors:

http://www.evolutionnews.org/2009/05/do ... 20491.html

Speaking of the rise of new genes,

Scientists decipher 3 billion-year-old genomic fossils where it says,

CAMBRIDGE, Mass. — MIT scientists have created a sort of genomic fossil that shows that the collective genome of all life underwent an enormous expansion about 3 billion years ago, which they're calling the Archean Expansion. Many of the new genes appearing in the Archean Expansion are oxygen related, and could be the first biological evidence of the Great Oxidation Event, the period in Earth's history when oxygen became so plentiful that many anerobic life forms may have become extinct. A report of this work by Eric Alm and Lawrence David will appear in Nature online Dec. 19.

(my bold) etc etc. Nature link is here.

Shrunk wrote:
The closest thing to a response from the DI I could find is this. Predictably, they don't actually acknowledge that they cannot answer the challenge, but instead just come up with excuses and non-sequitors:

http://www.evolutionnews.org/2009/05/do ... 20491.html

Disapointingly, the whole thing seems to be nothing more than a plug to sell Meyer's forthcoming book.

Weaver wrote:

Behe’s implicit conclusion was that evolution in nature—and not just in bacteria and viruses, but all species—also occurred in this way; that is, brand-new genes or genetic elements (he calls them “FCTs”) could not originate de novo by mutation and natural selection, but had to be put there by the Intelligent Designer (aka God/Jebus). Behe did not, and could not, say this in the paper, but intelligent-design advocates certainly touted this conclusion (see here and here, for instance), and now Behe himself has said the same thing on his blog at Uncommon Descent:

Behe wrote:. . . I was saying that, no matter what causes gain-of-FCT events to sporadically arise in nature (and I of course think the more complex ones likely resulted from deliberate intelligent design http://tinyurl.com/32n64xl), short-term Darwinian evolution will be dominated by loss-of-FCT, which is itself an important, basic fact about the tempo of evolution.

Note that here he doesn‘t limit this conclusion (which he conveniently omitted from the QRB paper) to bacteria and viruses.

In that case, Behe needs to read more scientific papers. Because the literature on de novo gene origination is expansive. This list of papers that I've known about for some time probably represents less than 1% of the available literature:

De Novo Origination Of A New Protein-Coding Gene In Saccharomyces cerevisiae by Jing Cai, Ruoping Zhao, Huifeng Jiang and Wen Wang, Genetics, 179: 487-496 (May 2008) [full paper downloadable from here]

Extensive De Novo Genomic Variation In Rice Introduced By Introgression From Wild Rice (Zizania latifolia Griseb.) by Yong-Ming Wang, Zhen-Ying dong, Zhoing-Juan Zhang, Xiu-Yun Lin, Ye Shen, Daowei Zhou and Bao Liu, Genetics, 170: 1945-1956 (August 2005) [full paper downloadable from here]

Novel Genes Derived From Noncoding DNA In Drosophila melanogaster Are Frequently X-Linked And Exhibit Testis-based Expression by Mia T. Levine, Corbin D. Jones, Andrew D. Kern, Heather A. Lindfors and David J. Begun, Proceedings of the National Academy of Sciences of the USA, 103(26): 9935-9939 (27th June 2006) [full paper downloadable from here]

Evidence For De Novo Evolution Of Testis-Expressed Genes In The Drosophila yakuba/Drosophila erecta Clade by David J. Begun, Heather A. Lindfors, Andrew D. Kern and Corbin D. Jones, Genetics, 176: 1131-1137 (June 2007) [full paper downloadable from here]

Evolution Of Enzymes For The Metabolism Of New Chemical Inputs Into The Environment by Lawrence P. Wackett, Journal of Biological Chemistry, 279(40): 41259-41264 (1st October 2004) [full paper downloadable from here]

Evolution Of Hydra, A Recently Evolved Testis-Expressed Gene With Nine Alternative First Exons In Drosophila melanogaster by Shou-Tao Chen, Hsin-Chien Cheng, Daniel A. Barbash and Hsiao-Pei Yang, PLoS Genetics, 3(7): 1131-1143 (July 2007) [full paper downloadable from her]

Recently Evolved Genes Identified From Drosophila yakuba And D. erecta Accessory Gland Expressed Sequence Tags by David J. Begun, Heather A. Lindfors, Melissa E. Thompson and Alisha K. Holloway, Genetics, 172: 1675-1681 (March 2006) [full paper downloadable from here]

Oh well, I just glanced at the paper without much enthusiasm anyway. By Behe's standards, it is relatively objective!

Darwinsbulldog wrote:Oh well, I just glanced at the paper without much enthusiasm anyway. By Behe's standards, it is relatively objective!

A couple initial thoughts of my own:

Behe's paper is a useful tool with which to bitch slap any creationists who trot out the "no beneficial mutations" canard, since here is a paper by one of their own admitting that they exist.

I also wonder if Behe can provide any observed examples, under natural conditions, of his claimed mechanism of beneficial mutations being inserted into a genome by an "intelligent designer"?

I think we'll see a lot more papers like this. The formula is,

Start by citing or quoting the "THE ORIGIN OF SPECIES" by Darwin (1859) and being careful not to quotemine but picking up some point it is making. Follow this by lots of science stuff. Finish with some doubts or questions for further research.

The hope is that people will read the first paragraph, the conclusion and then decide that Darwin and the scientific position has holes in it.

Darwinsbulldog wrote:


To play the devil's advocate for a second, I just noticed that Michael Behe has brought out a serious paper:-

http://www.lehigh.edu/~inbios/pdf/Behe/QRB_paper.pdf

.

Calilasseia wrote:

In that case, Behe needs to read more scientific papers. Because the literature on de novo gene origination is expansive. This list of papers that I've known about for some time probably represents less than 1% of the available literature:

Thanks for these references, will work through.

As I understand Behe's argument loss of function mutations are by far and away the most common occurrence and where gain of function appears this can most often be explained by reactivation of dormant coding sequences - probably by loss of function of repressor genes. The ID group can then claim that evolution works backwards - getting rid of unnecessary protein encoding rather than creating novel proteins.

I have yet to fully understand the literature on 'de novo' gene origination, but the most recent paper quoted seemed to be at thel level of arguing that because no examples of similar codes had been found to date within related population, they must be de novo. A reasonable start, but I suspect a weight of literature supporting this from multiple different species will probably be necessary to win the argument - perhaps that is already available?

Calilasseia wrote: De Novo Origination Of A New Protein-Coding Gene In Saccharomyces cerevisiae by Jing Cai, Ruoping Zhao, Huifeng Jiang and Wen Wang, Genetics, 179: 487-496 (May 2008) [full paper downloadable from here]

The link seems to be incorrect there. Here is the correct one:

http://www.genetics.org/cgi/reprint/179/1/487

Pebble wrote:As I understand Behe's argument loss of function mutations are by far and away the most common occurrence and where gain of function appears this can most often be explained by reactivation of dormant coding sequences - probably by loss of function of repressor genes. The ID group can then claim that evolution works backwards - getting rid of unnecessary protein encoding rather than creating novel proteins.

It seems to me there is a more basic conceptual problem with Behe's idea: His distinction between "gain of function" and "modification of function". While that might make some sense generally, in terms of promoting ID over evolution (assuming that is his true motivation in writing this paper ) I think he oversells this idea. What I think he wants to imply is that only "gain of function" mutations would confirm evolution as a plausible mechanism for speciation and other major phenotypic changes. But it seems to me successive cumulative "modifications" by themselves are sufficient to explain this. If we think of the type of morphological changes we observe thru the fossil record, modification of existing structure by far predominates over the emergence of novel structures. I'm not sure I can even think of an example of the latter. Fins gradually become legs which gradually become wings or arms. Fins, legs, wings and arms don't just emerge "de novo." There's no reason to require that "emergence de novo" occur at the molecular level, either.

Shrunk wrote:

It seems to me there is a more basic conceptual problem with Behe's idea: His distinction between "gain of function" and "modification of function". While that might make some sense generally, in terms of promoting ID over evolution (assuming that is his true motivation in writing this paper ) I think he oversells this idea.

I'm less sure - as defined below, I think this is a very honest and fair way of interpreting a modification of function.

"Another population indigenous to some
malarial regions has a different point mutation
in their hemoglobin. In this instance,
the sixth codon of the
chain has
mutated from glutamic acid to lysine. Although
the altered hemoglobin (HbC)
does not aggregate as sickle hemoglobin
does, it confers resistance to malaria for
reasons that are unclear. Because apparently
no new, discrete, coded molecular
feature has been developed, this is categorized
as a “modification-of-function” adaptive
mutation; no FCT has been lost or
gained."


As to the inferences then drawn - that is a different matter. One can certainly propose that functionally equivalent alleles can still create differences over time and it would appear that there is good evidence for that. However, modifications that change a fin to an arm would certainly not fit this mould, that would definitely require some change in function. To assert that equivalent alleles lead to such changes requires evidence somewhere along the line for a gain or loss of function.

Pebble wrote:

Shrunk wrote:

It seems to me there is a more basic conceptual problem with Behe's idea: His distinction between "gain of function" and "modification of function". While that might make some sense generally, in terms of promoting ID over evolution (assuming that is his true motivation in writing this paper ) I think he oversells this idea.

I'm less sure - as defined below, I think this is a very honest and fair way of interpreting a modification of function.

"Another population indigenous to some
malarial regions has a different point mutation
in their hemoglobin. In this instance,
the sixth codon of the
chain has
mutated from glutamic acid to lysine. Although
the altered hemoglobin (HbC)
does not aggregate as sickle hemoglobin
does, it confers resistance to malaria for
reasons that are unclear. Because apparently
no new, discrete, coded molecular
feature has been developed, this is categorized
as a “modification-of-function” adaptive
mutation; no FCT has been lost or
gained."

I'm not sure how that relates to my point.

As to the inferences then drawn - that is a different matter. One can certainly propose that functionally equivalent alleles can still create differences over time and it would appear that there is good evidence for that. However, modifications that change a fin to an arm would certainly not fit this mould, that would definitely require some change in function. To assert that equivalent alleles lead to such changes requires evidence somewhere along the line for a gain or loss of function.

So where does the "change in function" occur in the above? it all looks like modifications to me.

Shrunk,

Isn't the base function of all limb forms retained, that being the locomotion of the organism, even though the morphology has undergone drastic alteration?

RS

theropod wrote:Shrunk,

Isn't the base function of all limb forms retained, that being the locomotion of the organism, even though the morphology has undergone drastic alteration?

RS

That's what I'm saying. At the morphological level, and therefore also at the genetic level, all that is happening at each stage is a modification of an existing structure. However, the cumulative effect of all this is a significant change in function (from swimming to crawling to walking to flying or to performing a Beethoven piano sonata). At no point is one of Behe's "FTC's" required. All that happens is the shape and proportions of the various individual bones are modified.

Pebble seems to think otherwise, however, if I understand him correctly.

As I read it, Behe was careful to distinguish between the molecular function and the phenotypic function. The phenotype might have a function, but Behe was restricting his paper to only molecular function, which might not seem to apply at the level of a whole limb (as there may be a number of molecular functions affecting a limb). I don't know a whole lot about genetics in detail so the following illustration may not be a good one, but in terms of what Behe was discussing, if a mutation occurred that prevented an inhibitor from activating due to a point mutation, preventing restriction of size of a limb part for example then Behe would consider that a loss of function mutation, even if the change in size allowed a new morphological function, e.g. allowing a fin to be used for propulsion along the bottom, or to be impressive to attract a mate, as well as a previous function of steering while swimming.

However, at the molecular level would it be easier to identify a loss of function, since a function is already known, than to determine gain of function, where a function for the new form would need to be determined? Could this influence the ratio of loss to gain observed in the studies? In a similar way deleterious mutations in humans may be better known because they are relevant to medicine and appear as medical problems, whereas beneficial mutations may be harder to identify.

Shrunk wrote:

theropod wrote:Shrunk,

Isn't the base function of all limb forms retained, that being the locomotion of the organism, even though the morphology has undergone drastic alteration?

RS

That's what I'm saying. At the morphological level, and therefore also at the genetic level, all that is happening at each stage is a modification of an existing structure. However, the cumulative effect of all this is a significant change in function (from swimming to crawling to walking to flying or to performing a Beethoven piano sonata). At no point is one of Behe's "FTC's" required. All that happens is the shape and proportions of the various individual bones are modified.

Pebble seems to think otherwise, however, if I understand him correctly.

Cool. I thought I read you correctly, and agree completely.

RS

sam_j wrote:As I read it, Behe was careful to distinguish between the molecular function and the phenotypic function. The phenotype might have a function, but Behe was restricting his paper to only molecular function, which might not seem to apply at the level of a whole limb (as there may be a number of molecular functions affecting a limb). I don't know a whole lot about genetics in detail so the following illustration may not be a good one, but in terms of what Behe was discussing, if a mutation occurred that prevented an inhibitor from activating due to a point mutation, preventing restriction of size of a limb part for example then Behe would consider that a loss of function mutation, even if the change in size allowed a new morphological function, e.g. allowing a fin to be used for propulsion along the bottom, or to be impressive to attract a mate, as well as a previous function of steering while swimming.

Well, that's just the point, isn't it? I fail to see how this helps the creationist cause. If he is trying to argue that evolution won't work without God, because only God can produce "FTC's" or whatever Behe wants to call them, it entirely undercuts his position to remind everyone that non-"FTC" mutations can still produce beneficial changes.

Any time they have to sharpen the wedge it's a good thing.