Kong Yoon-Ju, Joo Jeong-Hwan, Kim Keun Pil, Hong Soogil
Department of Life Sciences, Chung-Ang University, Seoul 06974, Republic of Korea.
J Microbiol Biotechnol. 2017 Feb 28;27(2):405-411. doi: 10.4014/jmb.1610.10074.
Homologous recombination occurs between homologous chromosomes and is significantly involved in programmed double-strand break (DSB) repair. Activation of two recombinases, Rad51 and Dmc1, is essential for an interhomolog bias during meiosis. Rad51 participates in both mitotic and meiotic recombination, and its strand exchange activity is regulated by an inhibitory factor during meiosis. Thus, activities of Rad51 and Dmc1 are coordinated to promote homolog bias. It has been reported that Hed1, a meiosis-specific protein in budding yeast, regulates Rad51-dependent recombination activity. Here, we investigated the role of Hed1 in meiotic recombination by ectopic expression of the protein after pre-meiotic replication in . DNA physical analysis revealed that the overexpression of Hed1 delays the DSB-to-joint molecule (JM) transition and promotes interhomolog JM formation. The study indicates a possible role of Hed1 in controlling the strand exchange activity of Rad51 and, eventually, meiotic crossover formation.
同源重组发生在同源染色体之间，并且在程序性双链断裂（DSB）修复中发挥着重要作用。两种重组酶Rad51和Dmc1的激活对于减数分裂期间的同源偏向至关重要。Rad51参与有丝分裂和减数分裂重组，并且其链交换活性在减数分裂期间受到抑制因子的调节。因此，Rad51和Dmc1的活性相互协调以促进同源偏向。据报道，芽殖酵母中的减数分裂特异性蛋白Hed1调节Rad51依赖性重组活性。在此，我们通过在减数分裂前复制后异位表达该蛋白来研究Hed1在减数分裂重组中的作用。DNA物理分析表明，Hed1的过表达延迟了DSB到联合分子（JM）的转变，并促进了同源JM的形成。该研究表明Hed1在控制Rad51的链交换活性以及最终减数分裂交叉形成中可能发挥的作用。
