Studies of meiotic recombination have revealed an evolutionary paradox. Molecular and genetic analysis has shown that crossing over initiates at specifiec sites called hotspots, by a recombinational-repair mechanism in which the initiating hotspot is replaced by a copy of its homolog. Under this scenario active hotspot alleles will rapidly be replaced by inactive alleles, which arise by mutations and increase by recombination-associated gene conversion. A previous model (Boulton et al, 1997 aka the BMR-model) have shown that neither the benefits of accurate segregation nor those of recombining flanking genes are sufficient to preserve the active alleles in the face of conversion. Recent evidence from molecular studies have characterize recombinational hotspots in greater detail and have significantly modified our view of the molecular mechanism of recombination. We now know that hotspot activity is regulated by one or several trans-acting modifier loci. Futhermore, the hotspot sites are associated with structurally compromised regions of the chromatin which are predominantly located in promoter regions. We have revisited the BMR-model and incoporated this new molecular evidence into a multilocus modifier model using a genetic algorithm in an attempt to resolve the paradox.

Reference: Boulton et al. 1997. The hotspot conversion paradox and the evolution of meiotic recombination. PNAS 94:8058-8063

The paper is available at http://penguin.zoology.ubc.ca/reprints/boulton_etal97.pdf