Modulation of prdm9-controlled meiotic chromosome asynapsis overrides hybrid sterility in mice

0Citations
Citations of this article
38Readers
Mendeley users who have this article in their library.

Abstract

Hybrid sterility is one of the reproductive isolation mechanisms leading to speciation. Prdm9, the only known vertebrate hybrid-sterility gene, causes failure of meiotic chromosome synapsis and infertility in male hybrids that are the offspring of two mouse subspecies. Within species, Prdm9 determines the sites of programmed DNA double-strand breaks (DSBs) and meiotic recombination hotspots. To investigate the relation between Prdm9-controlled meiotic arrest and asynapsis, we inserted random stretches of consubspecific homology on several autosomal pairs in sterile hybrids, and analyzed their ability to form synaptonemal complexes and to rescue male fertility. Twenty-seven or more megabases of consubspecific (belonging to the same subspecies) homology fully restored synapsis in a given autosomal pair, and we predicted that two or more DSBs within symmetric hotspots per chromosome are necessary for successful meiosis. We hypothesize that impaired recombination between evolutionarily diverged chromosomes could function as one of the mechanisms of hybrid sterility occurring in various sexually reproducing species.

Cite

CITATION STYLE

APA

Gregorova, S., Gergelits, V., Chvatalova, I., Bhattacharyya, T., Valiskova, B., Fotopulosova, V., … Forejt, J. (2018). Modulation of prdm9-controlled meiotic chromosome asynapsis overrides hybrid sterility in mice. ELife, 7. https://doi.org/10.7554/eLife.34282

Register to see more suggestions

Mendeley helps you to discover research relevant for your work.

Already have an account?

Save time finding and organizing research with Mendeley

Sign up for free