Where gynodioecy is cast out of God’s creation

Finally, I am a real person (not another anonymous “somebody”).

A rebuttal of sorts of the long-standing case of T-urf13 as an example that refutes many different pillars of ID thought has been posted on Evolution News. The essay is authored by “Evolution News”, which, as far as I am concerned, means it is coauthored by all of the contributors to the blog. (I state this in case anyone wonders why I cite Behe et al. in the following as the authors of this essay.) There are many things about the essay that deserve discussion, and I will try to get to them over the next few days or weeks. Accordingly, this is the first of several posts. I will not be following the ENV piece in order, but will jump around (in seemingly random fashion, as it were).

The argument I will discuss in this post is the claim that T-urf13 causes male sterility and also susceptibility to a fungal toxin, and is thus a deleterious feature. For some reason (not well-articulated by the ENV crew), this in some way invalidates my claims about protein evolution. I say that the point raised by the ENV crew is irrelevant – T-urf13 is a completely new gene and protein, the core of an irreducibly complex system, and something that arose totally from non-coding DNA via well-understood enzymatic mechanisms. The phenotypic consequences of the appearance of T-urf13 are rather beside the point.

But there is more to this interesting story. Behe et al. (the ENV coauthors) state:

A further point that needs to be noted is that the phenotype is in fact harmful, not beneficial, to the organism. It results both in male sterility and susceptibility to the fungal toxin. T-urf13 would probably never persist in a natural context and only does persist because it has been artificially selected for by humans who want to breed corn strains with male sterility.

The emphasized statement is essentially an assertion that cytoplasmic male sterility could never persist (or, I am guessing, arise) in nature. This would come as a great surprise to plant biologists. Plants, as readers here probably know, reproduce sexually, through the union of male and female gametes. However, there is a dizzying range of approaches that plants take towards sexual reproduction. In some species, all individuals may be hermaphrodites, possessing both male and female sexual organs. In other species, individuals may be either male or female. In yet others, there may be mixtures of hermaphrodites and females. This latter group of plants are called gynodioecious. In gynodioecious plants, females are male sterile, often (but not always) via mechanisms that recall those that underlie male sterility in cms-T corn. I emphasize – these plants exist in the wild, and thus necessarily cytoplasmic male sterility is a trait that persists in nature. In other words, Behe et al. are quite incorrect in their suppositions about cytoplasmic male sterility.

Behe et al. go on to make some odd claims about the stability of the trait by referring to a study of cell cultures derived from cmsT corn:

In fact, one of the major reasons we know that T-urf13 is responsible for cytoplasmic male sterility and disease susceptibility is the presence of revertant mutations that delete the T-urf13 gene in cell culture experiments where cms-T maize is grown on a medium containing BmT toxin, rendering the plants disease resistant and male fertile. What’s surprising, however, is that when those experiments were repeated without toxin selection, occasional revertant mutations were nonetheless obtained. These results suggest that the T-urf13 gene confers a selective disadvantage that is independent of sensitivity to the BmT toxin (Pring et al., 1988).

What Behe et al. omit is the opening sentence of the paragraph from Pring et al. that discusses these results:

Although the expression of CMS in T-cytoplasm is stable under normal field conditions , tissue culture of T-cytoplasm maize apparently provides the appropriate conditions to induce or allow genetic changes to occur and be recovered as culture lines and in regenerated plants.

What Pring et al. are discussing is the use of tissue culture to rapidly generate mutations that alter the cmsT trait. Importantly, they note, at the very beginning of the paragraph that the ENV autors are paraphrasing, that male sterility in cmsT corn is stable under normal field conditions. Contrast this with the assertion of the ENV authors:

T-urf13 would probably never persist in a natural context …

Behe et al. continue:

…one hypothesis that has been proposed for how T-urf13 causes male sterility is that T-urf13 results in a decrease in the efficiency of mitochondrial activity, and that this causes the plants to be incapable of attaining the threshold of ATP production that is necessary for the development of pollen (Levings, 1993). Note that this is a loss-of-function change.

But caused by a completely new protein and IC system. We need to keep our eyes on the prize – new protein, new IC system, an increase in information, etc.

Skipping a section in which the authors badly misunderstand the concept of restorer mutations and genotypes (which are, as a matter of fact, yet more instances of the addition of new functionality via normal mutational processes), Behe et al. conclude this section thusly:

It is thus quite telling that, as their flagship example of a new protein complex arising de novo, Arthur Hunt, Nathan Lents, and others choose to promote a system that in fact causes harm to the organism that bears it.

By now, it should not be lost on readers that ENV is in essence claiming that gynodioecious plants are somehow in harm’s way or under some sorts of evolutionary or ecological stress. And that, in essence, they cannot really persist or even exist in nature. The fact of the matter is that cytoplasmic sterility, in the wild and in the corn field, affords distinctive advantages to the plant. To claim that this trait causes harm is to badly misunderstand many aspects of plant biology.

@pnelson, you should have asked Richard Buggs to review and revise this essay before you approved it; Buggs would, I am sure, have corrected some of these notions and probably provided a more nuanced and challenging discussion of the trait and the implications for protein evolution.

(For those who may not be aware of this, growing plant cells in culture is a well-known way to generate mutations, sort of akin to chemical or radiation-induced mutagenesis. This is because plant cells can be prone to substantial chromosomal rearrangements when passed through culture. This is a source of what are called somaclonal variants or mutants and have been used as genetic and breeding tools for decades.)


It would be interesting to hear about other examples of cytoplasmic male sterility that are persisting in nature. As a physician, I have a lot to learn about plants. Maybe been learning about humans all these years.

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But is anyone surprised that they would make such blatantly, objectively false assumption?


I’d just like to add that humans are a part of other organism’s “natural context”, and therefore selection pressures imparted by humans in no way invalidates the persistence of certain mutations that result therefrom. If the T-urf13 mutations are adaptively beneficial in the context of human breeders selecting for male sterility, then T-urf13 is beneficial. Period.

There is probably no such thing as an unconditionally beneficial mutation. Polar bear adaptations would probably not persist in tropical rain forests.