SYCP3 regulates strand invasion activities of RAD51 and DMC1

被引：21
|
作者：
Kobayashi, Wataru [1 ]
Hosoya, Noriko [2 ]
Machida, Shinichi [1 ]
Miyagawa, Kiyoshi [2 ]
Kurumizaka, Hitoshi [1 ,3 ]
机构：
[1] Waseda Univ, Grad Sch Adv Sci & Engn, Lab Struct Biol, Shinjuku Ku, 2-2 Wakamatsu Cho, Tokyo 1628480, Japan
[2] Univ Tokyo, Grad Sch Med, Ctr Dis Biol & Integrat Med, Lab Mol Radiol, Tokyo 1138655, Japan
[3] Waseda Univ, Inst Med Oriented Struct Biol, Shinjuku Ku, 2-2 Wakamatsu Cho, Tokyo 1628480, Japan
来源：
GENES TO CELLS | 2017年 / 22卷 / 09期
关键词：
MEIOTIC RECOMBINATION; SYNAPTONEMAL COMPLEX; CHROMOSOME SYNAPSIS; SACCHAROMYCES-CEREVISIAE; MECHANISTIC INSIGHTS; PARTNER CHOICE; RECA HOMOLOG; C-TERMINUS; PROTEIN; MEIOSIS;
D O I：
10.1111/gtc.12513
中图分类号：
Q2 [细胞生物学];
学科分类号：
071009 ; 090102 ;
摘要：
The synaptonemal complex is a higher-ordered proteinaceous architecture formed between homologous chromosomes. SYCP3 is a major component of the lateral/axial elements in the synaptonemal complex and is essential for meiotic recombination. Previous genetic studies showed that SYCP3 functions in meiotic homologous recombination biased to interhomologous chromosomes, by regulating the strand invasion activities of the RAD51 and DMC1 recombinases. However, the mechanism by which SYCP3 regulates RAD51- and DMC1-mediated strand invasion remains elusive. In this study, we found that SYCP3 significantly suppresses the RAD51-mediated, but not the DMC1-mediated, strand invasion reaction by competing with HOP2-MND1, which is an activator for both RAD51 and DMC1. A SYCP3 mutant with defective RAD51 binding does not inhibit the RAD51-mediated homologous recombination in human cells. Therefore, SYCP3 may promote the DMC1-driven homologous recombination by attenuating the RAD51 activity during meiosis.
引用
收藏
页码：799 / 809
页数：11
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