Počet záznamů: 1
Histone methyltransferase PRDM9 is not essential for meiosis in male mice
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SYSNO ASEP 0521508 Druh ASEP J - Článek v odborném periodiku Zařazení RIV J - Článek v odborném periodiku Poddruh J Článek ve WOS Název Histone methyltransferase PRDM9 is not essential for meiosis in male mice Tvůrce(i) Mihola, Ondřej (UMG-J) RID, ORCID
Pratto, F. (US)
Brick, K. (US)
Linhartová, Eliška (UMG-J)
Kobets, Tetyana (UMG-J) RID
Flachs, Petr (UMG-J)
Baker, C.L. (US)
Sedláček, Radislav (UMG-J) RID
Paigen, K. (US)
Petkov, P.M. (US)
Camerini-Otero, R.D. (US)
Trachtulec, Zdeněk (UMG-J) RID, ORCIDCelkový počet autorů 12 Zdroj.dok. Genome Research. - : Cold Spring Harbor Laboratory Press - ISSN 1088-9051
Roč. 29, č. 7 (2019), s. 1078-1086Poč.str. 9 s. Forma vydání Online - E Jazyk dok. eng - angličtina Země vyd. US - Spojené státy americké Klíč. slova double-strand breaks ; recombination hotspots ; localization ; infertility ; speciation ; asynapsis ; musculus ; strains ; drive ; gene Vědní obor RIV EB - Genetika a molekulární biologie Obor OECD Reproductive biology (medical aspects to be 3) CEP GA14-20728S GA ČR - Grantová agentura ČR GA16-06548S GA ČR - Grantová agentura ČR LM2015040 GA MŠMT - Ministerstvo školství, mládeže a tělovýchovy ED1.1.00/02.0109 GA MŠMT - Ministerstvo školství, mládeže a tělovýchovy LO1419 GA MŠMT - Ministerstvo školství, mládeže a tělovýchovy ED2.1.00/19.0395 GA MŠMT - Ministerstvo školství, mládeže a tělovýchovy Způsob publikování Open access Institucionální podpora UMG-J - RVO:68378050 UT WOS 000473730600004 DOI 10.1101/gr.244426.118 Anotace A hallmark of meiosis is the rearrangement of parental alleles to ensure genetic diversity in the gametes. These chromosome rearrangements are mediated by the repair of programmed DNA double-strand breaks (DSBs) as genetic crossovers between parental homologs. In mice, humans, and many other mammals, meiotic DSBs occur primarily at hotspots, determined by sequence-specific binding of the PRDM9 protein. Without PRDM9, meiotic DSBs occur near gene promoters and other functional sites. Studies in a limited number of mouse strains showed that functional PRDM9 is required to complete meiosis, but despite its apparent importance, Prdm9 has been repeatedly lost across many animal lineages. Both the reason for mouse sterility in the absence of PRDM9 and the mechanism by which Prdm9 can be lost remain unclear. Here, we explore whether mice can tolerate the loss of Prdm9. By generating Prdm9 functional knockouts in an array of genetic backgrounds, we observe a wide range of fertility phenotypes and ultimately demonstrate that PRDM9 is not required for completion of male meiosis. Although DSBs still form at a common subset of functional sites in all mice lacking PRDM9, meiotic outcomes differ substantially. We speculate that DSBs at functional sites are difficult to repair as a crossover and that by increasing the efficiency of crossover formation at these sites, genetic modifiers of recombination rates can allow for meiotic progression. This model implies that species with a sufficiently high recombination rate may lose Prdm9 yet remain fertile. Pracoviště Ústav molekulární genetiky Kontakt Nikol Škňouřilová, nikol.sknourilova@img.cas.cz, Tel.: 241 063 217 Rok sběru 2020 Elektronická adresa https://genome.cshlp.org/content/29/7/1078
Počet záznamů: 1