Modulation of Prdm9-controlled meiotic chromosome asynapsis overrides hybrid sterility in mice

0497019 - ÚMG 2019 RIV GB eng J - Journal Article
Gregorová, Soňa - Gergelits, Václav - Chvátalová, Irena - Bhattacharyya, Tanmoy - Vališková, Barbora - Fotopulosová, Vladana - Jansa, Petr - Wiatrowska, Diana - Forejt, Jiří
Modulation of Prdm9-controlled meiotic chromosome asynapsis overrides hybrid sterility in mice.
eLife. Roč. 7, Marz (2018), č. článku e34282. ISSN 2050-084X. E-ISSN 2050-084X
R&D Projects: GA ČR GA13-08078S; GA MŠMT(CZ) LQ1604
Institutional support: RVO:68378050
Keywords : histone h3 methyltransferase * mismatch repair system * strand break formation * reproductive isolation * mammalian meiosis * escherichia-coli * gene-expression * mouse * recombination * speciation
OECD category: Genetics and heredity (medical genetics to be 3)
Impact factor: 7.551, year: 2018

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.
Permanent Link: http://hdl.handle.net/11104/0289649