RTEL-1 Enforces Meiotic Crossover Interference and Homeostasis

被引:136
作者
Youds, Jillian L. [1 ]
Mets, David G. [2 ]
McIlwraith, Michael J. [3 ]
Martin, Julie S. [1 ]
Ward, Jordan D. [1 ]
ONeil, Nigel J. [4 ]
Rose, Ann M. [4 ]
West, Stephen C. [3 ]
Meyer, Barbara J. [2 ]
Boulton, Simon J. [1 ]
机构
[1] Canc Res UK, London Res Inst, DNA Damage Response Lab, S Mimms EN6 3LD, Herts, England
[2] Univ Calif Berkeley, Howard Hughes Med Inst, Dept Mol & Cell Biol, Berkeley, CA 94720 USA
[3] Canc Res UK, London Res Inst, Genet Recombinat Lab, S Mimms EN6 3LD, Herts, England
[4] Univ British Columbia, Fac Med, Dept Med Genet, Vancouver, BC V6T 1Z4, Canada
关键词
CAENORHABDITIS-ELEGANS; STRAND-EXCHANGE; C-ELEGANS; RECOMBINATION; CHROMOSOME; PROTEINS; YEAST;
D O I
10.1126/science.1183112
中图分类号
O [数理科学和化学]; P [天文学、地球科学]; Q [生物科学]; N [自然科学总论];
学科分类号
07 ; 0710 ; 09 ;
摘要
Meiotic crossovers (COs) are tightly regulated to ensure that COs on the same chromosome are distributed far apart ( crossover interference, COI) and that at least one CO is formed per homolog pair (CO homeostasis). CO formation is controlled in part during meiotic double-strand break (DSB) creation in Caenorhabditis elegans, but a second level of control must also exist because meiotic DSBs outnumber COs. We show that the anti-recombinase RTEL-1 is required to prevent excess meiotic COs, probably by promoting meiotic synthesis-dependent strand annealing. Two distinct classes of meiotic COs are increased in rtel-1 mutants, and COI and homeostasis are compromised. We propose that RTEL-1 implements the second level of CO control by promoting noncrossovers.
引用
收藏
页码:1254 / 1258
页数:5
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