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Forsdyke, D. R.

Publications and source records attributed to Forsdyke, D. R..

2 recordsLinked to original sources

Prdm9 is an Anti-Speciation Gene

Mechanisms initiating a branching process that can lead to new species are broadly classified as chromosomal and genic. Chromosomal mechanisms are supported by breeding studies involving exchanges of individual chromosomes or their segments between mouse subspecies. There are also studies of the rapidly mutating mouse PR/SET-domain 9 (prdm9) gene, which encodes PRDM9, a protein targeting DNA recombination hotspots. When PRDM9 is bound symmetrically with equal strength, the meiotic repair of mutations in one parental strand, based on information on the allelic strand (conversion), would seem to be unbiased in discriminating between strands. So mismatches detected between pairing paternal and maternal DNA strands (heteroduplexes) undergo unbiased conversions (to homoduplexes). This leaves uncertainty on whether a mutation has been corrected or compounded. However, it has been hypothesized that tagging of mismatch regions, so that both strands are epigenetically marked as uncertain, would make it possible over numerous generations for mutations to be corrected (biased conversions) whenever asymmetry is detected. Thus, variation would decrease and members of a species would remain within its bounds. Intriguingly, new experimental studies show that, when chromosomally interpreted, PRDM9 also works through asymmetrical epigenetic labelling to confine members to species bounds. To the extent that the experimentally observed and hypothetical anti-speciation asymmetries can be related, chromosomal mechanisms are further supported.

evolutionary biology

Base composition, speciation, and why the mitochondrial barcode precisely classifies

While its mechanism and biological significance are unknown, the utility of a short mitochondrial DNA sequence as a \"barcode\" providing accurate species identification has revolutionized the classification of organisms. Since highest accuracy was achieved with recently diverged species, hopes were raised that barcodes would throw light on the speciation process. Indeed, a failure of a maternally-donated, rapidly mutating, mitochondrial genome to coadapt its gene products with those of a paternally-donated nuclear genome could result in developmental failure, thus creating a post-zygotic barrier leading to reproductive isolation and sympatric branching into independent species. However, the barcode itself encodes a highly conserved, species-invariant, protein, and the discriminatory power resides in the non-amino acid specific bases of synonymous codons. It is here shown how the latter could register changes in the oligonucleotide frequencies of nuclear DNA that, when they fail to match in pairing meiotic chromosomes, could reproductively isolate the parents (whose hybrid is sterile) so launching a primary divergence into two species. It is proposed that, while not itself contributing to speciation, the barcode sequence provides an index of the nuclear DNA oligonucleotide frequencies that drive speciation.

evolutionary biology