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In vivo binding of PRDM9 reveals interactions with noncanonical genomic sites
被引:50
作者:
Grey, Corinne
[1
]
Clement, Julie A. J.
[1
]
Buard, Jerome
[1
]
Leblanc, Benjamin
[2
]
Gut, Ivo
[3
,4
]
Gut, Marta
[3
,4
]
Duret, Laurent
[5
]
de Massy, Bernard
[1
]
机构:
[1] Univ Montpellier, CNRS, UMR9002, Inst Genet Humaine, F-34396 Montpellier 05, France
[2] Univ Copenhagen, BRIC, DK-2200 Copenhagen, Denmark
[3] BIST, CRG, CNAG CRG, Barcelona 08028, Spain
[4] UPF, Barcelona 08003, Spain
[5] Univ Claude Bernard, Univ Lyon, CNRS, Lab Biometrie & Biol Evolut,UMR 5558, F-69100 Villeurbanne, France
基金:
欧洲研究理事会;
关键词:
STRAND BREAK FORMATION;
MEIOTIC RECOMBINATION INITIATION;
REPAIR PATHWAY CHOICE;
H3;
LYSINE;
36;
HOMOLOGOUS RECOMBINATION;
CHROMOSOME SYNAPSIS;
GENE CONVERSION;
MOUSE GENOME;
DNA;
MICE;
D O I:
10.1101/gr.217240.116
中图分类号:
Q5 [生物化学];
Q7 [分子生物学];
学科分类号:
071010 ;
081704 ;
摘要:
In mouse and human meiosis, DNA double-strand breaks (DSBs) initiate homologous recombination and occur at specific sites called hotspots. The localization of these sites is determined by the sequence-specific DNA binding domain of the PRDM9 histone methyl transferase. Here, we performed an extensive analysis of PRDM9 binding in mouse spermatocytes. Unexpectedly, we identified a noncanonical recruitment of PRDM9 to sites that lack recombination activity and the PRDM9 binding consensus motif. These sites include gene promoters, where PRDM9 is recruited in a DSB-dependent manner. Another subset reveals DSB-independent interactions between PRDM9 and genomic sites, such as the binding sites for the insulator protein CTCF. We propose that these DSB-independent sites result from interactions between hotspot-bound PRDM9 and genomic sequences located on the chromosome axis.
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页码:580 / 590
页数:11
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