Chromosome-wide characterization of meiotic noncrossovers (gene conversions) in mouse hybrids.
PRDM9 motif erosion
gene conversion
homologous recombination
hybrid sterility
noncrossover-associated GC bias
Journal
Genetics
ISSN: 1943-2631
Titre abrégé: Genetics
Pays: United States
ID NLM: 0374636
Informations de publication
Date de publication:
03 03 2021
03 03 2021
Historique:
received:
23
09
2020
accepted:
13
11
2020
entrez:
8
3
2021
pubmed:
9
3
2021
medline:
13
8
2021
Statut:
ppublish
Résumé
During meiosis, the recombination-initiating DNA double-strand breaks (DSBs) are repaired by crossovers or noncrossovers (gene conversions). While crossovers are easily detectable, noncrossover identification is hampered by the small size of their converted tracts and the necessity of sequence polymorphism. We report identification and characterization of a mouse chromosome-wide set of noncrossovers by next-generation sequencing of 10 mouse intersubspecific chromosome substitution strains. Based on 94 identified noncrossovers, we determined the mean length of a conversion tract to be 32 bp. The spatial chromosome-wide distribution of noncrossovers and crossovers significantly differed, although both sets overlapped the known hotspots of PRDM9-directed histone methylation and DNA DSBs, thus supporting their origin in the standard DSB repair pathway. A significant deficit of noncrossovers descending from asymmetric DSBs proved their proposed adverse effect on meiotic recombination and pointed to sister chromatids as an alternative template for their repair. The finding has implications for the molecular mechanism of hybrid sterility in mice from crosses between closely related Mus musculus musculus and Mus musculus domesticus subspecies.
Identifiants
pubmed: 33683354
pii: 5998651
doi: 10.1093/genetics/iyaa013
pmc: PMC8045703
doi:
Substances chimiques
Histone-Lysine N-Methyltransferase
EC 2.1.1.43
prdm9 protein, mouse
EC 2.1.1.43
Types de publication
Journal Article
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
1-14Informations de copyright
© The Author(s) 2020. Published by Oxford University Press on behalf of Genetics Society of America. All rights reserved. For permissions, please email: journals.permissions@oup.com.
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