Hays S L, Firmenich A A, Berg P
Department of Biochemistry, Stanford University School of Medicine, Stanford University, CA 94305, USA.
Proc Natl Acad Sci U S A. 1995 Jul 18;92(15):6925-9. doi: 10.1073/pnas.92.15.6925.
The repair of DNA double-strand breaks in Saccharomyces cerevisiae requires genes of the RAD52 epistasis group, of which RAD55 and RAD57 are members. Here, we show that the x-ray sensitivity of rad55 and rad57 mutant strains is suppressible by overexpression of RAD51 or RAD52. Virtually complete suppression is provided by the simultaneous overexpression of RAD51 and RAD52. This suppression occurs at 23 degrees C, where these mutants are more sensitive to x-rays, as well as at 30 degrees C and 36 degrees C. In addition, a recombination defect of rad55 and rad57 mutants is similarly suppressed. Direct in vivo interactions between the Rad51 and Rad55 proteins, and between Rad55 and Rad57, have also been identified by using the two-hybrid system. These results indicate that these four proteins constitute part of a complex, a "recombinosome," to effect the recombinational repair of double-strand breaks.
酿酒酵母中DNA双链断裂的修复需要RAD52上位性组的基因,其中RAD55和RAD57是该组的成员。在此,我们表明,rad55和rad57突变株对X射线的敏感性可通过过表达RAD51或RAD52来抑制。RAD51和RAD52的同时过表达几乎能完全抑制这种敏感性。这种抑制在23摄氏度(这些突变株对X射线更敏感)、30摄氏度和36摄氏度时均会发生。此外,rad55和rad57突变株的重组缺陷也受到类似的抑制。通过双杂交系统还鉴定出了Rad51与Rad55蛋白之间以及Rad55与Rad57之间直接的体内相互作用。这些结果表明,这四种蛋白质构成了一个复合体(“重组体”)的一部分,以实现双链断裂的重组修复。