Does a "500 million-year-old hormone" disprove Darwin?

In a paper published by the FASEB Journal in 1999, Danielle Georges and Christian Schwabe described gene sequences from the tunicate Ciona intestinalis that were indistinguishable from porcine relaxin (1). Newer data contradict that finding: recently published analyses of the C. intestinalis genome do not confirm the presence of relaxin sequences (2). What might seem like a narrow issue of scientific fact has broader implications. To the delight of creationists and fans of intelligent design, the presence of similar relaxin sequences in pigs and sea squirts–species separated by 500 million years–has been used to cast genomic doubt on Darwinian evolution. Indeed, Schwabe has repeatedly cited the tunicate relaxin data, and the nearly identical relaxin sequences he has identified in whales, (3) not only to support his own “Genomic Potential Hypothesis” but also to refute modern evolutionary biology (4). Schwabe’s hypothesis would replace Darwin’s theory of common descent with the view of the independent origin of all species, thereby making the origin of life and the origin of species one and the same problem. Moreover, the “Genomic Potential Hypothesis” rejects natural selection of random variations as the mechanism that underlies speciation and adaptation. Thus, albeit Schwabe sees chemistry as the sole force generating genomes and species the independent origin of all species asserted by his “Genomic Potential Hypothesis” coincides with the creationist view of the origin of species. Since Schwabe therefore is regularly cited by creationists as an “atheistic scientist” who rejects neoDarwinism, it seems worthwhile to critique his experimental work in the context of his “Genomic Potential Hypothesis.” It’s an hypothesis that wants to have it both ways. On the one hand, Schwabe argues that the high degree of diversity found in the relaxin sequences of different species would date speciation events much earlier than phylogenies based on other data. On the other hand, he argues that the identity of tunicate, cetacean, and porcine relaxin sequences cannot be explained by Darwinian selection of random mutants. This concomitant use of sequence diversity and sequence identity to deny the theory of evolution appears to us at least curious or at worst tautologous. The 1999 The FASEB Journal paper immediately evoked critical responses summarized by an editor’s comment (5) that the conclusions rested entirely on PCR and microsequencing data, two methods quite prone to contamination. The authors rejected those concerns and replied that the experiments were carried out in two separate labs and that Georges had never worked with porcine material before (6). Not so: Georges had indeed used polyA -RNA from pregnant sow ovaries (the organ in which relaxin is produced) in work published well before The FASEB Journal paper (7). At any rate, since the genomic sequence was reported to lack introns, the cDNA could have served as a good probe for Southern blot analysis of genomic DNA, a far more robust technique (a description of Southern blot analysis appears in the Methods section of The FASEB Journal paper but such data are not presented in the Results section). Indeed, this approach would have enabled the authors to decide whether the sequence variation they observed in one tenth of the PCR products was introduced during amplification, whether it resulted from a polymorphism of the gene or if two different relaxin genes reside within the Ciona genome as the authors speculated. In point of fact, polymorphisms would contradict the “Genomic Potential Hypothesis,” because, as rigidly interpreted, the Schwabe hypothesis would predict the independent origins of individuals carrying different alleles (see below). Still, the authors adduce the fact that Ciona relaxin is more similar to an infrequent allele of porcine relaxin. They suggest an “occasional exchange” in the respective position of the porcine gene: but that of course implies a mutation. Curiously, Schwabe willingly accepts that “chance mutations” may cause inherited human diseases (8) but denies that mutations can drive evolution. In addition it should be