Multiple losses of aKRAB from PRDM9 coincide with a teleost-specific intron size distribution

In mammals, PRDM9 defines the sites of meiotic recombination through a mechanism that increases structural variance and depends on aKRAB. The loss of aKRAB is likely to have shifted the locations of both recombination and structural variance hotspots. Our observations suggest that the TD evolved as a side-effect of these changes and link recombination to the evolution of intron size illustrating how genome architectures can evolve in the absence of selection.