Shinohara M, Shita-Yamaguchi E, Buerstedde J M, Shinagawa H, Ogawa H, Shinohara A
Department of Biology, Graduate School of Science, Osaka University, Toyonaka, Japan.
Genetics. 1997 Dec;147(4):1545-56. doi: 10.1093/genetics/147.4.1545.
The RAD54 gene, which encodes a protein in the SWI2/SNF2 family, plays an important role in recombination and DNA repair in Saccharomyces cerevisiae. The yeast genome project revealed a homologue of RAD54, RDH54/TID1. Properties of the rdh54/tid1 mutant and the rad54 rdh54/tid1 double mutant are shown for mitosis and meiosis. The rad54 mutant is sensitive to the alkylating agent, methyl methanesulfonate (MMS), and is defective in interchromosomal and intrachromosomal gene conversion. The rdh54/tid1 single mutant, on the other hand, does not show any significant deficiency in mitosis. However, the rad54 rdh54/tid1 mutant is more sensitive to MMS and more defective in interchromosomal gene conversion than is the rad54 mutant, but shows the same frequency of intrachromosomal gene conversion as the rad54 mutant. These results suggest that RDH54/TID1 is involved in a minor pathway of mitotic recombination in the absence of R4D54. In meiosis, both single mutants produce viable spores at slightly reduced frequency. However, only the rdh54/tid1 mutant, but not the rad54 mutant, shows significant defects in recombination: retardation of the repair of meiosis-specific double-strand breaks (DSBs) and delayed formation of physical recombinants. Furthermore, the rad54 rdh54/tid1 double mutant is completely defective in meiosis, accumulating DSBs with more recessed ends than the wild type and producing fewer physical recombinants than the wild type. These results suggest that one of the differences between the late stages of mitotic recombination and meiotic recombination might be specified by differential dependency on the Rad54 and Rdh54/Tid1 proteins.
RAD54基因编码SWI2/SNF2家族中的一种蛋白质,在酿酒酵母的重组和DNA修复中发挥重要作用。酵母基因组计划揭示了RAD54的一个同源物RDH54/TID1。展示了rdh54/tid1突变体和rad54 rdh54/tid1双突变体在有丝分裂和减数分裂中的特性。rad54突变体对烷化剂甲磺酸甲酯(MMS)敏感,在染色体间和染色体内基因转换方面存在缺陷。另一方面,rdh54/tid1单突变体在有丝分裂中未表现出任何明显缺陷。然而,rad54 rdh54/tid1突变体比rad54突变体对MMS更敏感,在染色体间基因转换方面缺陷更大,但染色体内基因转换频率与rad54突变体相同。这些结果表明,在没有R4D54的情况下,RDH54/TID1参与有丝分裂重组的一条次要途径。在减数分裂中,两个单突变体产生可育孢子的频率略有降低。然而,只有rdh54/tid1突变体,而不是rad54突变体,在重组中表现出明显缺陷:减数分裂特异性双链断裂(DSB)修复延迟和物理重组体形成延迟。此外,rad54 rdh54/tid1双突变体在减数分裂中完全缺陷,积累的DSB末端比野生型更凹陷,产生的物理重组体比野生型少。这些结果表明,有丝分裂重组后期和减数分裂重组后期之间的差异之一可能由对Rad54和Rdh54/Tid1蛋白的不同依赖性决定。