In another thread , I mentioned that the ENV discussion of T-urf13 (Does T-urf13 Refute Irreducible Complexity? A Response to Arthur Hunt | Evolution News) as it relates to protein evolution was “jaw-droppingly bad”. I have already pointed out how Behe et al. in effect write off all gynodioecious plants as unfit, something that is bad enough. But other parts of the essay are worse.
In keeping with the PR push to explain evolution in terms of devolution, Behe et al. devote one section to the argument that T-urf13 actually arose by degradation of a pre-existing protein-coding gene. I reproduce the relevant section in its entirety here:
Origins of T-urf13 Likely Involves Loss-of-Function
If T-urf13 is usually deleterious, and persists mainly due to man’s artificial selection, how, then, did it arise? Everyone agrees that it arose by chance. But did it arise de novo or, instead, does it represent the devolution of some pre-existing gene? Rather than T-urf13 having arisen in “one fell swoop,” it seems more likely that its origin involves a loss-of-function scenario, consistent with what Behe writes in Darwin Devolves and previously in The Edge of Evolution (Behe, 2007; Behe, 2019).
As noted, T-urf13, which is found only in this sub-strain of corn, has similarity to URF-13, which is found more widely in native corn. One possible scenario is that the URF-13 complex is involved in some other process, and that it became broken such that it was no longer properly regulated. Indeed, the first identification of T-urf13 long pre-dates the sequencing of the maize genome in the early 2000s (Chandler and Brendel, 2002; Schnable et al., 2009; Soderlund et al., 2009; Gore et al., 2009; Vielle-Calzada et al. 2009). It thus was impossible to determine whether the T-urf13 gene had indeed arisen de novo “from scratch,” or whether it was already present and doing something else. Is there any evidence to support such a hypothesis? For one thing, as already mentioned, T-urf13 appears to be under the regulation of a nuclear-encoded protein, namely, Rf2 (Cui et al., 1996). This seems to suggest that T-urf13 may have been previously involved in other processes.
Proteins embedded in the mitochondrial membrane are synthesized in the cytosol, and therefore they possess an alpha helical aphipathic coil at the N-terminus that is recognized by transport complexes (see this section from the textbook Molecular Biology of the Cell for details). It follows that there ought to be a signal peptide for mitochondrial membrane insertion. That implies that what we have is actually an insertion of DNA into a pre-existing gene that was itself a membrane protein for mitochondria and perhaps a channel — and perhaps a regulated channel since it is affected by nuclear genes. A tool called Signal-BLAST, available at the website of the Center for Applied Molecular Engineering (CAME), allows a user to identify signal peptides in a protein sequence (Frank and Sippl, 2008). Entering the FASTA file for T-urf13 yields a result output of a signal peptide, putative cleavage site after AA 35 (by similarity to RLF32_ARATH). RLF32_ARATH is a signal peptide for import into mitochondria for a gene in Arabidopsis. That protein is involved in cell-cell signaling by way of Ca++ influx. What all this means is that T-urf13 probably came from a fully functional, pre-existing gene, and did not arise de novo.
This section is, to say the least, stunning in its combined use of fabrication, avoidance of plan-as-day fact, and understanding of cell biology. To begin with:
As noted, T-urf13, which is found only in this sub-strain of corn, has similarity to URF-13, which is found more widely in native corn.
Um, no. This is entirely fabricated. The protein we are speaking of is unique to the mitochondrial genome of cmsT maize. There is no “URF13” that is found more widely in native corn. (Behe et al. say that this similarity is “as noted”, but they don’t actually note this anywhere in the essay.). This claim is totally and completely a fabrication, something that Behe et al. have pulled from out of thin air, with absolutely no supporting data or evidence. (It may be that Behe et al. may have come across other genes named as URF13 in some searches of the NCBI databases. This is a term that others have used for other genes. But none of the items Behe et al. may have found are relevant to T-urf13.)
Indeed, the first identification of T-urf13 long pre-dates the sequencing of the maize genome in the early 2000s (Chandler and Brendel, 2002; Schnable et al., 2009; Soderlund et al., 2009; Gore et al., 2009; Vielle-Calzada et al. 2009). It thus was impossible to determine whether the T-urf13 gene had indeed arisen de novo “from scratch,” or whether it was already present and doing something else.
This statement is also stunning . Behe et al. seem to be implying that before the advent of DNA sequencing, we could know nothing about genes, inheritance, and other genetics subjects. In so doing, they completely ignore the fact that, long before DNA sequencing was possible, the scientific community knew that the T-urf13 gene was resident in the mitochondrial genome, and this was accomplished using traditional, old-fashioned genetics analyses. The scientific community also knew that there were physical differences between normal and cmsT mitochondrial genomes that could be unambiguously linked with the cmsT trait, thanks to the application of restriction enzyme mapping to the characterization of the maize mitochondrial genome. DNA sequencing only finished the story, and leaves no doubt as to the origins of the gene. None whatsoever.
I will skip over the bizarre claims about T-urf13 and nuclear restorers, except to state that nuclear restorers of fertility in male-sterile corn (generally speaking, not just in the case of cmsT corn) are collectively additional examples of the evolution of new protein functionality. Why Behe et al. mention this here is hard to understand.
So, what is the “evidence” for a devolutionary origin of T-urf13?
Proteins embedded in the mitochondrial membrane are synthesized in the cytosol, and therefore they possess an alpha helical aphipathic coil at the N-terminus that is recognized by transport complexes (see this section from the textbook Molecular Biology of the Cell for details). It follows that there ought to be a signal peptide for mitochondrial membrane insertion. That implies that what we have is actually an insertion of DNA into a pre-existing gene that was itself a membrane protein for mitochondria and perhaps a channel — and perhaps a regulated channel since it is affected by nuclear genes. A tool called Signal-BLAST, available at the website of the Center for Applied Molecular Engineering (CAME), allows a user to identify signal peptides in a protein sequence (Frank and Sippl, 2008).
Yet another passage that defies description. Behe et al. are correct in the pointer they include for the description of mitochondrial targeting (or transit) peptides. However, the computational tool (Signal-BLAST) they use to identify such a sequence in T-urf13 actually analyzes sequences for a different sort of signal peptide, one that is recognized by the SRP complex. It is not trained on organellar transit peptides and thus will miss them. Which means that the (very limited) homology that Behe et al. detect is completely irrelevant to the model they propose.
Entering the FASTA file for T-urf13 yields a result output of a signal peptide, putative cleavage site after AA 35 (by similarity to RLF32_ARATH). RLF32_ARATH is a signal peptide for import into mitochondria for a gene in Arabidopsis. That protein is involved in cell-cell signaling by way of Ca++ influx. What all this means is that T-urf13 probably came from a fully functional, pre-existing gene, and did not arise de novo.
The piece-de-resistance, as it were. Behe et al. are proposing that T-urf13 arose from a nuclear gene, possibly (this sentence is somewhat vague) encoding a Ca channel related to RLF32. In so doing, they are claiming that the extremely low sequence similarity they see is more compelling than the high homology of T-urf13 with other parts of the maize mitochondrial genome. Basically, because they use a tool that is inappropriate for their aim, they are pulling one more piece of “evidence” from out of thin air.
To summarize, Behe et al. dismiss a long, storied, and highly effective tradition of genetic analysis (in corn, in this case), they completely fabricate “genes” that they need for their devolutionary scenario, and they confuse two different fundamental cell biological mechanisms. This is what I mean by “jaw-droppingly bad”.
