Now that we have discussed the shortcoming of Meyer’s… revised… history and his sloppy research (again), let’s talk about some science!
So, where do new genes come from?
Meyer says this:
These studies typically begin by taking a gene and then seeking to find other genes that are similar (or homologous) to it. They then seek to trace the history of slightly different homologous genes back to a hypothetical common ancestor gene (or genes).
and
Some studies also attempt to establish the existence of a common ancestor gene on the basis of similar genes within the very same organism. They then typically propose evolutionary scenarios in which an ancestral gene duplicates itself,12 and then the duplicate and the original evolve differently as the result of subsequent mutations in each gene.
That note 12 is a reference to note 15 in Chapter 10.
So, is this what actually happens? Let’s look at some papers that Meyer ignores. Like this one “The evolution of the novel Sdic gene cluster in Drosophila melanogaster by Rita Ponce and Daniel Hartl.[1] (PDF) This was published in 2006, well before Darwin’s Doubt was published. I find it interesting since even a basic search on “evolution” “novel” “gene” should find this paper. I wonder why Meyer keeps ignoring papers that are directly relevant to his work.
This is the first paragraph in that paper.
Genomic analysis has revealed the prevalence of gene duplications in eukaryotes. While the presence of similar genes in genomes was already known from protein sequencing studies in the late 1950s, the study of whole genomes has shown that about one-third of eukaryotic genomes is comprised of duplicated genes and multi-gene families (e.g. Rubin et al., 2000). The mean duplication rate was estimated at 0.01 per gene per MY , a surprisingly high rate of the same order of magnitude as the per-nucleotide mutation rate (Lynch and Conery, 2000).
Let me be very clear. This is a huge topic. For example, that first paper (Rubin, PDF) was
A comparative analysis of the genomes of Drosophila melanogaster, Caenorhabditis elegans, and Saccharomyces cerevisiae and the proteins they are predicted to encode was undertaken in the context of cellular, developmental, and evolutionary processes.
For the record, that’s a fruit fly, a worm, and a yeast that they are comparing the genomes of. Something else that Meyer neglects. But the conclusion of this paper gives Meyer and other ID proponents a chance. Here it is:
First, the core proteome sizes of flies and worms are similar and are only twice the size of that of yeast. This is perhaps counterintuitive, because the fly, a multicellular animal with specialized cell types, complex development, and a sophisticated nervous system, looks more than twice as complicated as single-celled yeast. The lesson is that the complexity apparent in the metazoans is not achieved by sheer number of genes (54). Second, there has been a proliferation of bigger and more complex proteins in the two metazoans relative to yeast, including, not surprisingly, more proteins with extracellular domains involved in cell-cell and cell-substrate interactions. Finally, the population of multidomain proteins is somewhat larger and more diverse in the fly than in the worm. There is presently no practical way to quantify differences in biological complexity between two organisms, however, so it is not possible to correlate this increased domain expansion and diversity in the fly with differences in development and morphology.
I highlighted the important bit. There you go ID proponents. There’s your chance to show us. If you can quantify the differences in complexity between two organisms, then you will have succeeded in impressing us and started to make headway into the real world. But we all know you can’t do it.
The reason that is such a big deal is that the genome of the fly, a multicellular animal, is the same size as that of the worm, which is multicellular, but has not respiratory or circulatory system. And both are only twice the size of the single-celled yeast. But what is even more interesting occurs when comparing the two genomes.
Comparative analysis of the predicted proteins encoded by these genomes suggests that nearly 30% of the fly genes have putative orthologs in the worm genome. We required that a protein show significant similarity over at least 80% of its length to a sequence in another species to be considered its ortholog (6). We know that this results in an underestimate, because the length requirement excludes known orthologs, such as homeodomain proteins, which have little similarity outside the homeodomain.
Over 30% of the genome between the fly and the worm are effectively the same gene. Common ancestry is shown in orthologs (among other things). That’s what creationists just don’t get. There isn’t ONE thing that supports common ancestry, there are dozens of totally unique things that support common ancestry.
OK, I’ve digressed, because that’s pretty cool. Mainly the result is that unlike what Meyer and some other creationists, massive amounts of new genes are not required to form wildly different organisms. I don’t know if Meyer actually thinks this, so I’ll leave it alone for now. So, on to new genes.
Here’s an article[2] that Meyer missed and is directly relevant to Meyer’s claim that
Upon closer examination, however, none of these papers demonstrate how mutations and natural selection could find truly novel genes or proteins in sequence space in the first place; nor do they show that it is reasonably probable (or plausible) that these mechanisms would do so in the time available.
You mean the 50+ million years of the Cambrian explosion? Considering that Homo sapiens didn’t exist a mere 6 million years ago, that should be plenty of time. Indeed, it was plenty of time because we actually see the fossils.
Let’s see what Lynch says about this.
It is now well established that the genomes of most eukary0tic organisms contain thousands of gene produced by an array of events, including tandem duplication of single genes, replicative translocation, chromosomal duplication, and polyploidization. For example, 40%-50% of the genes in the nematode Caenorhabditis elegans and in the fly Drosophila melanogaster are recognizable duplicates of various ages (Rubin et al. 2000). The genomes of virtually all vertebrates (Nadeau and Sankoff 1997; Postlethwait et al. 1998) contain two or more copies of gene family members for large numbers of functional proteins. Genomic analyses suggest that the members of the great ape lineage (humans, gorillas, and chimpanzees), which diverged only 5 Ma, differ substantially in terms of the numbers and locations of duplicate genes (Pennisi 1998); and similar inferences have been made for the congeneric nematodes C. elegans and Caenorhabditis briggsae (Robertson 1998). A complete analysis of human chromosome 22 revealed several duplicated regions separated by substantial physical distances (Dunham et al. 1999). Probably at least one-third of all flowering plants and even higher proportions of mosses and ferns are polyploid derivatives (Lewis 1980), and most diploid plants also carry many duplicate loci (Gottlieb 1982). The relatively streamlined genome of Arabidopsis thaliana contains large numbers of gene duplicates (Lin et al. 1999; Mayer et al. 1999); many of these duplicates are tandemly arrayed, but there are also several examples of replicative translocation of chromosomal regions containing dozens to hundreds of genes, and the species may have even experienced an ancient genome duplication event (Grant et al. 2000). [my emphasis[
Note that this paper was written in 2000, 13 years before Darwin’s Doubt and all the references are before that. So what we have here is a list (with references to peer reviewed literature) that shows the examples of gene duplications. Hey look, there’s our pals Rubin et. al that we’ve already mentioned that shows that half the genes in the nematode and the fly are duplicates. A paper that isn’t in Meyer’s book. Indeed, after searching through the book, none of these papers are referenced. So, Meyer has not referenced a single paper (out of dozens) that disputes his claim. In fact, continuing to review these types of papers, Lynch and Force, Rubin and Long appear to be the leaders in this field, each with several papers that talk about gene duplication and the generation of novel genes… yet Meyer doesn’t reference a single paper by any of them.
Let’s go back to the Ponce and Hart paper since it directly discusses the evidence for gene duplications.
A case in point is the Sdic gene described by Nurminsky et al. (1998a,b). This is a new gene that has evolved very recently in D. melanogaster that exists in all wild strains of D. melanogaster, but is not present in the other sibling species (Nurminsky et al., 1998b). Hence Sdic evolved and was fixed in the last 2–3 million years, the time D. melanogaster split from its closest related species (Caccone et al., 1988), which makes Sdic a very recent gene.
How do we know that this gene resulted from duplications?
The Sdic gene encodes a novel protein, a sperm-specific dynein intermediate chain, one of the proteins involved in sperm tail movement (Nurminsky et al., 1998b). Sdic is a chimera: it is composed of parts of two other genes, AnnX and Cdic, which also exist as intact copies in the genome flanking the region that includes Sdic (Nurminsky et al., 1998b). From its structure, it was possible to deduce that Sdic was formed by duplication, deletions, and other rearrangements (Nurminsky et al., 1998b). The 5′ UTR of this new gene derives from AnnX, a gene that encodes a cell adhesion protein, and all the transcribed part derives from the Cdic gene, a gene that encodes a cytoplasmic dynein intermediate chain. The protein encoded by Sdic is a dynein resembling the one encoded by Cdic but truncated at the N-terminal end (Nurminsky et al., 1998a,b). The promoter elements derive from the fusion of these two genes, including a region that was previously an exon, forming a promoter de novo that confers testis-specific expression on the gene (Nurminsky et al., 1998b).
Another comment about duplication.
Southern blot analysis indicate that Sdic is duplicated several times in this region of the genome (Nurminsky et al., 1998b).
So scientists have actually seen the same gene in different places in the genome. Duplications happen. The other papers detail (see Lynch) detail how a gene duplication can allow for mutations to affect one gene while retaining the function of the original. In some cases, resulting in speciation.
Interestingly, the Ponce and Hart paper do not use the method described in Darwin’s Doubt. Of course, the method that Meyer describes so glibbly in two paragraphs takes up nearly a full page of text in the relevant papers. What did Ponce and Hart find?
We found four copies of the Sdic gene present in region 19 of the X chromosome of D. melanogaster. These four genes are located in tandem between the genes Cdic and AnnX. These four genes are complete copies, that is, are not truncated, and except for small indels are all approximately the same size (5.3 kb). All genes are in the same orientation with each other and in the same orientation as Cdic and AnnX, in the minus (−) strand. The four Sdic genes were numbered sequentially from Sdic1 to 4, Sdic1 being the gene in the cluster closest to AnnX and thus to the centromere (Fig. 1). We found no other copy of this gene, or parts of this gene, in any other location in the genome.
But are they identical duplications?
The comparison of the nucleotide sequence of the four genes reveals several changes among them: besides nucleotide changes, the alignments require the incorporation of gaps indicating insertion and deletion events (Table 1). Some mutations are unique to one gene, but most changes are shared by more than one copy. In particular, most shared mutations are shared by the gene pair Sdic1 and Sdic3, and by the pair Sdic2 and Sdic4.
Hmmm… so a duplication event happened, some mutations occurred, then more duplication events happened. I guess one could hypothesize the idea of an intelligent designer being efficient by reusing code, but then one would have to actually have an intelligent designer.
So, what’s is happening here is that the copies are changing by known mutational effects. What are the results?
On the other hand, it may have been the high number of changes in Sdic1 that created the novel protein. The changes in Sdic1 happened since the split of the melanogaster/simulans lineages (in the last two million years) and there is evidence for positive selection of Sdic genes by at least one selective sweep (Nurminsky et al., 1998b; Nurmisnky et al., 2001; Kulathinal et al., 2004). Other novel gene functions recently described are frequently associated with rapid changes and show signs of positive selection (Long and Langley, 1993; Betrán and Long, 2003; Wang et al., 2002), which supports the idea of novel genetic functions allowing adaptive changes. In any case, Sdic1 is genetic novelty that is species specific, with male-specific expression encoding a new reproductive protein that may be playing a role in adaptation or sexual selection in D. melanogaster.
Wow six more references that support the claims in this paragraph. That the Sdic1 gene is species specific and a novel gene that produces a novel protein that may very well have resulted in the speciation in the fruit fly.
I cannot express how cool this is. First, it completely destroys Meyers entire book. That seems to be happening a lot actually.
The evidence presented in this paper and dozens of others that Meyer doesn’t even mention directly refute his claims. One more thing, then I’ll close.
Towards the end of this section (p 212 and 214) [3]Meyer makes a HUGE mistake.
None of the scenarios that the Long paper cites demonstrate the mathematical or experimental plausibility of the mutational mechanisms they assert as explanations for the origin of genes. Nor do they directly observe the presumed mutational processes in action. At best, they provide hypothetical, after-the-fact reconstructions of a few events out of a sequence of many supposed events, starting with the existence of a presumed common ancestor gene. But that gene itself does not represent a hard data point. It is inferred to have existed on the basis of the similarity of two or more other existing genes, which are the only actual pieces of observational evidence upon which these often elaborate scenarios are based.
That these scenarios depend on various inferences and postulations doesn’t, by itself, disqualify them from consideration. Nevertheless, whether they adequately explain the origin of genetic information depends upon the evidence for the existence of the entities they infer (the ancestral genes) and the plausibility of the mutational mechanisms they postulate.
That’s pretty damning (if it were true). But let’s try a little experiment shall we? I’m going to retype the above statements with a few minor changes (in bold).
None of the scenarios that the ID Proponents use demonstrate the mathematical or experimental plausibility of the design they assert as explanations for the origin of genes. Nor do they directly observe the presumed design processes in action. At best, they provide hypothetical, after-the-fact reconstructions of a few events out of a sequence of many supposed events, starting with the existence of a presumed designer. But that design itself does not represent a hard data point. It is inferred to have existed on the basis of the similarity of two or more other existing genes, which are the only actual pieces of observational evidence upon which these often elaborate scenarios are based. .
That these scenarios depend on various inferences and postulations doesn’t, by itself, disqualify them from consideration. Nevertheless, whether they adequately explain the origin of genetic information depends upon the evidence for the existence of the design they infer (the designer) and the plausibility of the design mechanisms they postulate.
Hmmm… interesting isn’t it? I suspect that this irony will be lost on ID Proponents.
In the next section we’ll see what the Long paper cites and see if Meyer’s claims in that regard are true. Honestly, it doesn’t matter because the results from the papers cited in this post are sufficient to reject Meyer’s claims. But for the sake of completeness, we have to look.
Keep in mind that the Long paper cites some 100+ additional papers, so it could take a while. But if I find even a single example, then Meyer is shown to be a liar… again.
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[1] Ponce, R. & Hartl, D. L. The evolution of the novel Sdic gene cluster in Drosophila melanogaster. Gene 376, (2006).
[2] Lynch, M. & Force, A. G. The origin of interspecific genomic incompatibility via gene duplication. The American Naturalist 156, 590–605 (2000).
[3] There’s one of those horrid hand drawn pictures on p213.
