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Cisplatin-induced DNA double-strand breaks promote meiotic chromosome synapsis in PRDM9-controlled mouse hybrid sterility
L. Wang, B. Valiskova, J. Forejt,
Language English Country England, Great Britain
Document type Journal Article, Research Support, Non-U.S. Gov't
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PubMed
30592461
DOI
10.7554/elife.42511
Knihovny.cz E-resources
- MeSH
- Cisplatin toxicity MeSH
- DNA Breaks, Double-Stranded drug effects MeSH
- Histone-Lysine N-Methyltransferase genetics metabolism MeSH
- Hybridization, Genetic MeSH
- Meiosis drug effects genetics MeSH
- Infertility, Male genetics MeSH
- Mice, Inbred C57BL MeSH
- DNA Repair MeSH
- Chromosome Pairing drug effects genetics MeSH
- Antineoplastic Agents toxicity MeSH
- Animals MeSH
- Check Tag
- Male MeSH
- Animals MeSH
- Publication type
- Journal Article MeSH
- Research Support, Non-U.S. Gov't MeSH
PR domain containing 9 (Prdm9) is specifying hotspots of meiotic recombination but in hybrids between two mouse subspecies Prdm9 controls failure of meiotic chromosome synapsis and hybrid male sterility. We have previously reported that Prdm9-controlled asynapsis and meiotic arrest are conditioned by the inter-subspecific heterozygosity of the hybrid genome and we presumed that the insufficient number of properly repaired PRDM9-dependent DNA double-strand breaks (DSBs) causes asynapsis of chromosomes and meiotic arrest (Gregorova et al., 2018). We now extend the evidence for the lack of properly processed DSBs by improving meiotic chromosome synapsis with exogenous DSBs. A single injection of chemotherapeutic drug cisplatin increased frequency of RPA and DMC1 foci at the zygotene stage of sterile hybrids, enhanced homolog recognition and increased the proportion of spermatocytes with fully synapsed homologs at pachytene. The results bring a new evidence for a DSB-dependent mechanism of synapsis failure and infertility of intersubspecific hybrids.
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