DMC1 functions in a Saccharomyces cerevisiae meiotic pathway that is largely independent of the RAD51 pathway.
DMC1 functions in a Saccharomyces cerevisiae meiotic pathway that is largely independent of the RAD51 pathway.
复制标题
DMC1 在酿酒酵母减数分裂途径中发挥作用，该途径很大程度上独立于 RAD51 途径。
DOI：
10.1093/genetics/147.2.533
复制
发表时间：
1997
期刊：
影响因子：
3.3
通讯作者：
Kodadek,T
中科院分区：
文献类型：
--
作者：
Dresser,ME;Ewing,DJ;Conrad,MN;Dominguez,AM;Barstead,R;Jiang,H;Kodadek,T
酵母菌Saccharomyces gleae中的减数分裂重组需要两个相似的recA样蛋白Dmc 1 p和Rad 51 p。筛选显性减数分裂突变体提供了DMC 1-G126 D，这是一种在保守的ATP结合位点（特别是A环基序）发生突变的显性等位基因，其赋予无效表型。一个隐性无效等位基因dmc 1-K69 E是DMC 1-G126 D的基因内抑制基因。与Dmc 1 p不同，Dmc 1-K69 Ep在双杂交试验中不同源地相互作用，尽管它确实与通过Dmc 1 p双杂交筛选鉴定的其他融合蛋白相互作用。与Rad 51 p不同，Dmc 1 p在双杂交试验中不与Rad 52 p或Rad 54 p相互作用。然而，Dmc 1 p确实与Tid 1 p（Rad 54 p同源物）、Tid 4p（Rad 16 p同源物）以及其他不与Rad 51 p相互作用的融合蛋白相互作用，这表明Dmc 1 p和Rad 51 p在单独的（尽管可能重叠）重组修复复合物中起作用。上位性分析表明，DMC 1和RAD 51在负责减数分裂重组的不同途径中发挥作用。综上所述，我们的研究结果与DMC 1的减数分裂特异性DNA双链断裂末端进入染色质的要求一致。有趣的是，由减数分裂DNA双链断裂形成的染色体片段在CHEF凝胶上的模式在DMC 1突变株中与在rad 50 S株中所见的不同。
Meiotic recombinationin the yeastSaccharomyces cerevisiaerequires two similar recA-like proteins, Dmc1p and Rad51p. A screen for dominant meiotic mutants providedDMC1-G126D, a dominant allele mutated in the conserved ATP-binding site (specifically, the A-loop motif) that confers a null phenotype. A recessive null allele,dmc1-K69E, was isolated as an intragenic suppressor ofDMC1-G126D. Dmc1-K69Ep, unlike Dmc1p, does not interact homotypically in a two-hybrid assay, although it does interact with other fusion proteins identified by two-hybrid screen with Dmc1p. Dmc1p, unlike Rad51p, does not interact in the two-hybrid assay with Rad52p or Rad54p. However, Dmc1p does interact with Tid1p, a Rad54p homologue, with Tid4p, a Rad16p homologue, and with other fusion proteins that do not interact with Rad51p, suggesting that Dmc1p and Rad51p function in separate, though possibly overlapping, recombinational repair complexes. Epistasis analysis suggests thatDMC1andRAD51function in separate pathways responsible for meiotic recombination. Taken together, our results are consistent with a requirement forDMC1for meiosis-specific entry of DNA double-strand break ends into chromatin. Interestingly, the pattern on CHEF gels of chromosome fragments that result from meiotic DNA double-strand break formation is different inDMC1mutant strains from that seen inrad50Sstrains.