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RTEL-1 执行减数分裂交叉干扰和动态平衡。

RTEL-1 enforces meiotic crossover interference and homeostasis.

机构信息

DNA Damage Response Laboratory, London Research Institute, Cancer Research UK, Clare Hall, South Mimms, EN6 3LD, UK.

出版信息

Science. 2010 Mar 5;327(5970):1254-8. doi: 10.1126/science.1183112.

DOI:10.1126/science.1183112
PMID:20203049
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC4770885/
Abstract

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 antirecombinase 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.

摘要

减数分裂交叉(COs)受到严格调控,以确保同一条染色体上的 CO 彼此远离(CO 干扰,COI),并且每对同源染色体至少形成一个 CO(CO 稳态)。在秀丽隐杆线虫的减数分裂双链断裂(DSB)形成过程中,部分 CO 的形成受到控制,但还必须存在第二个调控水平,因为减数分裂 DSB 的数量超过 CO。我们发现,抗重组酶 RTEL-1 对于防止过多的减数分裂 CO 是必需的,这可能是通过促进减数分裂合成依赖性链退火来实现的。在 rtel-1 突变体中,两种不同类型的减数分裂 CO 增加,COI 和稳态受到损害。我们提出 RTEL-1 通过促进非交叉来实现 CO 控制的第二个水平。

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