Similarity and difference between Rad51 and Dmc1, two RecA homologs

2022 Fiscal Year Final Research Report

• Project/Area Number: 18H02371
• Research Category: Grant-in-Aid for Scientific Research (B)
• Allocation Type: Single-year Grants
• Section: 一般
• Review Section: Basic Section 43010:Molecular biology-related
• Research Institution: Tokyo Institute of Technology
• Principal Investigator: Tsubouchi Hideo 東京工業大学, 科学技術創成研究院, 助教 (20283822)
• Project Period (FY): 2018-04-01 – 2022-03-31
• Keywords: 相同組換え / 減数分裂 / DNA二重鎖切断 / 分裂酵母 / RecAホモログ / Dmc1 / Rad51 / DNA修復

Outline of Final Research Achievements

The reaction of finding homology between DNA sequences and exchanging homologous regions is called homologous recombination and is ubiquitous in life. RecA and its family of proteins (RecA homologs) play a central role in homologous recombination. Many eukaryotes have two RecA homologs, Rad51 and Dmc1. While Rad51 is expressed in both somatic and meiotic cells, Dmc1 is expressed only during meiosis. In this study, we found that Dmc1 is activated by two types of accessory factors through different mechanisms: the Swi5-Sfr1 complex functions in the stabilization of Dmc1 presynaptic filaments, whereas the Hop2-Mnd1 complex strongly promotes the initiation reaction of DNA strand exchange The Hop2-Mnd1 complex is thought to strongly promote the initiation reaction of DNA strand exchange.

Free Research Field

分子遺伝学

Academic Significance and Societal Importance of the Research Achievements

相同組換えはDNA傷害修復に重要なだけでなく、遺伝情報を次世代に伝える上で根幹をなす減数分裂にも必須の機能を持つ。本研究では減数分裂期組換えに中心的役割を果たすDmc1の活性化メカニズムを明らかにした。具体的には２種類の補助因子であるHop2-Mnd1とSwi5-Sfr1が独自の働きによりDmc1を活性化するメカニズムを分子レベルで明らかにした。減数分裂期組換えが異常になると不妊や遺伝性疾患の原因となることが知られている。本研究で得られた知見が生殖異常の原因究明や症状改善の手がかりとなることが期待される。