Bacteriophages, Budding Yeast, and Behe’s Vindication

I think the absence of public Christians among them undermined their case in religious audiences too

I’m pretty sure that Wesley Elsberry, one of the founders of Panda’s Thumb, is a Christian.

4 Likes

I have been able to ascertain that he’s a theistic evolutionist. See here and here.

And apparently he describes himself as a Christian here (scroll down to the bottom of the post).

3 Likes

Thanks! I thought that was the case, but it’s good to have confirmation.

1 Like

Following up a bit more on this subject:

From @Agauger’s ENV Piece -

“In the years since that paper was published, many cases of beneficial loss-of-function mutations have come to light. With the acceleration of genome sequencing more and more evidence has been accumulating. In 2014, a review article appeared in a special volume of Genomics devoted to experimental evolution. It outlined what could be learned from the many genomic studies to date. Gregory Lang and Michael Desai described many “adaptive mutations,” meaning mutations that helped the organism or cell grow faster or reproduce more. One could also call these beneficial mutations, and they did. They noted this:

Most long-term evolution experiments thus far have been performed in bacteria or haploid yeast populations, where, in most environments, there exist a number of loss-of-function mutations that provide a selective advantage. Given the large target size for these types of mutations, loss-of-function mutations often predominate the spectra of mutations recovered from long-term evolution experiments. Some of these loss events are neutral, attributable to mutation accumulation in the absence of selection for function, such as the reduction of catabolic breadth in E. coli[17], [18], [43]. However, many loss-of-function mutations have been confirmed to provide a selective advantage. For instance sterility in yeast provides a selective advantage by eliminating unnecessary gene expression [41]. The availability of beneficial loss-of-function mutations and the large target size for these events ensure that these mutations will come to dominate experimental evolution over short time scales. Over long time scales or in specialized conditions, mutational spectra may shift towards gain of function mutations. In diploid populations, we may also see a shift in the mutational spectrum away from loss-of-function mutations, towards dominant or overdominant mutations [24], [54]. However, there is currently only limited data describing the mutations that occur during experimental evolution in diploids, leaving the exact nature of this shift unclear . [Emphasis added.]

The following paragraph that @Agauger omitted is of interest as well:

Mutations affecting gene dosage are common in experimental evolution, in particular under nutrient limitation. For example, in chemostat cultures, where growth is strongly limited by a single nutri- ent, mutations that increase the import of the limiting nutrient are favored. Evolution in sulfur-limited media leads to the specific amplification of the high-affinity sulfur transporter, SUL1 [27]. Evolution under glucose limitation selects for amplification of the hexose trans- porters [11,20,32], and nitrogen limitation selects for amplification of nitrogen transporters PUT4, DUR3, and DAL4 [31]. The fitness effects of these amplification events are on the order of 10%, roughly an order of magnitude more advantageous than the beneficial mutations observed in rich medium conditions. This existence of these large effect mutations, combined with the large population sizes, may partially explain why some of the smaller effect mutations observed in rich medium conditions are not found in chemostat evolution experiments.

What this mechanism - altering gene dosage – brings to mind is the greater issue of regulatory evolution. This greater issue includes subjects such as alteration of transcription factors and their networks, and also of small RNA-mediated regulatory networks. (Incidentally, CRISPR is a subset of small RNA regulatory mechanisms.) I would argue that, if one is going to be making sweeping claims about evolutionary trends that affect adaptation and morphological evolution (such as proposing “the First Rule of Adaptive Evolution”), regulatory evolution really cannot be ignored or pushed aside. Neither paper @Agauger cites in the ENV piece, nor Behe’s 2010 paper, mention these sorts of mechanisms.

All of which leads to a question for the privileged few (@NLENTS, @swamidass, @Agauger, @pnelson) who have access to Behe’s new book – in his book, does Behe discuss subjects such as the evolution of transcription networks, or microRNA regulation? If so, how does he classify the changes attendant with rewiring of the relevant networks? Gain, modification, or loss of function? (This question repeats, in a sense, the one I asked @Agauger above about CRISPR.)

Finally, in the ENV piece, @Agauger also takes a swipe at @swamidass :

“Note: Cancer is not a good model for asking this question in eukaryotes, because the gain-of-function mutations in cancer do not produce structures or traits that lead to anything beneficial for the organism.”

I don’t buy this for a second. @swamidass?

4 Likes

A gain of function is seen with an evolved beta-galactosidase:

There is still the example of T-urf13:

There is the gain of function mutation which led to black coat color in pocket mice:

There is the infamous frameshift mutation that produced the nylonase gene:

https://jb.asm.org/content/174/24/7948.short?related-urls=yes&legid=jb;174/24/7948

1 Like

Honestly, this bothered me, as well. The sudden out-of-context mention of cancer mutations seems like an uncalled-for sideswipe directed singly at @swamidass. And although these mutations are not beneficial to the host, this fact is largely irrelevant. These mutations are certainly beneficial for the tumor.

5 Likes

There is almost always some way to put a “loss of function” spin on adaptive change. Consider a collection of genes under inhibition during certain growth conditions, “loss of function” in the inhibitory regulatory element can cause upregulation of that whole host of downstream genes. For example, the inhibiting regulatory element is preventing expression of genes when oxygen is present, and those genes are enzymes that act on some carbon source.

At what resolution are we supposed to evaluate whether a mutation is gain or loss of function? At the level of particular molecules, or their phenotypic effects on the life of the organism? If the “loss of function” of the inhibitory effect of the regulatory element, caused expression of certain genes under conditions they were previously inhibited, have that “loss of function” not in turn caused a gain of function for the organism when oxygen is present? It can now metabolize that carbon source under aerobic conditions where before it could not.

Consider an analogous but reverse situation, where inhibition of expression is beneficial. A regulatory element responsible for initiating transcription of a transporter gene is rendered nonfunctional through loss of function mutation, causing the carrier organism to not import an antibiotic that would otherwise have killed the organism if imported. Now the organism has gained the ability to live in the presence of this antibiotic, but we can still call that a “loss of function”.

It is difficult to think of an example of a genetic change that could not be described as some sort of loss. Be that loss of function(at whatever “level” of resolution), loss of information, loss of complexity, loss of specificity, loss of promiscuity or loss of diversity. Someone committed to that kind of rhetoric will almost always be able to come up with some way to render evolutionary change as “devolutionary” instead.

Whales lost the ability to run around on land. Freshwater fish lost the ability to live in salt water, or surface dwelling fish lost the ability to live at great depth, and so on.

5 Likes

A post was split to a new topic: Is Cancer a Good Model of Evolution?

I agree. I guess that, taken apart from the context of ID, then the notion that evolutionary changes are often driven by loss-of-function alterations is not too surprising, or unknown, or unexpected. Interesting, to be sure. But not what I would promote to some sort of law or rule.

The problem for Behe as I see it is that, if he is going to classify changes in regulatory networks as loss-of-function, then he is necessarily granting that loss-of-function can lead to significant evolutionary changes, the sorts that ID proponents insist require new information. This is a contradiction, a paradox of sorts that I don’t think ID proponents can resolve.

3 Likes

A reasonable protest, Curtis. I think Ann acknowledges this. May I now throw in my own example?

In debates about global warming, the terms “denier” is frequently used with intended negative connotations. The idea conveyed (and deliberately so, in most cases) is that people who claim to doubt the proportion of warming caused by human emissions are “in denial”, i.e., they really, deep down, know the truth, but are wriggling to avoid admitting it, even to themselves. That is, to be a “denier” is to be intellectually dishonest. This is, of course, an unfair characterization of a large number of people who aren’t fully convinced regarding the causality behind global warming. The term “AGW skeptic” would be more neutral, since “skeptic” conveys only the bare idea of doubt, without the connotations of dishonest motivation that go with “denier.”

(Also, “climate change denier” compounds the prejudice, since many who fully accept that the earth has warmed, and therefore do not deny “climate change,” remain skeptical about the causality.)

Note that nothing I have said implies the rightness or wrongness of the AGW position. I’m merely talking about how words are used with an “edge” to put opponents in the wrong, when it should be only evidence and argument that puts someone in the wrong, not a sinister label pertaining to alleged motivations. So I don’t want to open up a debate on climate change at all. I’m merely adding a footnote to your comment about the dangers of prejudicial terminology.

This topic was automatically closed 3 days after the last reply. New replies are no longer allowed.