TY - JOUR T1 - <em>Prdm9</em> is an Anti-Speciation Gene JF - bioRxiv DO - 10.1101/170860 SP - 170860 AU - Donald R. Forsdyke Y1 - 2017/01/01 UR - http://biorxiv.org/content/early/2017/07/31/170860.abstract N2 - Mechanisms initiating a branching process that can lead to new species are broadly classified as chromosomal and genic. Chromosomal mechanisms were supported by breeding studies involving exchanges of individual chromosomes between mouse subspecies. There were 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) would undergo unbiased conversions (to homoduplexes). This would leave uncertainty on whether a mutation had been corrected or compounded. However, a hypothetical 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. ER -