Mouse ANKRD31 Regulates Spatiotemporal Patterning of Meiotic Recombination Initiation and Ensures Recombination between X and Y Sex Chromosomes.
IHO1
MEI4
PRDM9
REC114
genome integrity in the germline
hotspots
mammalian reproduction
meiosis
recombination between psuedoautosomal regions of sex chromosomes
recombinosome assembly on chromosome axis
Journal
Molecular cell
ISSN: 1097-4164
Titre abrégé: Mol Cell
Pays: United States
ID NLM: 9802571
Informations de publication
Date de publication:
06 06 2019
06 06 2019
Historique:
received:
27
09
2018
revised:
01
02
2019
accepted:
20
03
2019
pubmed:
20
4
2019
medline:
23
10
2019
entrez:
20
4
2019
Statut:
ppublish
Résumé
Orderly segregation of chromosomes during meiosis requires that crossovers form between homologous chromosomes by recombination. Programmed DNA double-strand breaks (DSBs) initiate meiotic recombination. We identify ANKRD31 as a key component of complexes of DSB-promoting proteins that assemble on meiotic chromosome axes. Genome-wide, ANKRD31 deficiency causes delayed recombination initiation. In addition, loss of ANKRD31 alters DSB distribution because of reduced selectivity for sites that normally attract DSBs. Strikingly, ANKRD31 deficiency also abolishes uniquely high rates of recombination that normally characterize pseudoautosomal regions (PARs) of X and Y chromosomes. Consequently, sex chromosomes do not form crossovers, leading to chromosome segregation failure in ANKRD31-deficient spermatocytes. These defects co-occur with a genome-wide delay in assembling DSB-promoting proteins on autosome axes and loss of a specialized PAR-axis domain that is highly enriched for DSB-promoting proteins in wild type. Thus, we propose a model for spatiotemporal patterning of recombination by ANKRD31-dependent control of axis-associated DSB-promoting proteins.
Identifiants
pubmed: 31000436
pii: S1097-2765(19)30226-6
doi: 10.1016/j.molcel.2019.03.022
pii:
doi:
Substances chimiques
Carrier Proteins
0
Types de publication
Journal Article
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
1069-1085.e11Informations de copyright
Copyright © 2019 Elsevier Inc. All rights reserved.