Rao B S, Reddy N M
Mutat Res. 1982 Aug;95(2-3):213-24. doi: 10.1016/0027-5107(82)90259-7.
The gamma-radiation response of stationary and budding cells of wild-type diploid strains (RAD) and radiation-sensitive strains rad2, 6, 9, 18, 50-55, 57 and rec4 was studied. As compared with the wild-type strains, mutants generally showed enhanced sensitivity in both stages of the cell cycle. Budding-cell resistance was totally absent from rad50-55 strains. Mutants rad6, 9 and 18 showed some degree of budding-cell resistance. The response of rad2 and rec4 strains was identical with that of the corresponding wild-type strains. These results suggest that the pathway dependent upon the expression of RAD50-55 loci functions more efficiently in budding cells compared with the pathway dependent on RAD2 and RAD6, 9 and 18 loci. Recombination between sister chromatids appears to play an important role in budding-cell resistance, and this process is under the control of the RAD52 repair pathway. The relationship between the repair pathways associated with budding-cell resistance and post-irradiation cellular recovery (LHR) is discussed.
研究了野生型二倍体菌株（RAD）以及辐射敏感菌株rad2、6、9、18、50 - 55、57和rec4的静止期细胞和出芽期细胞对γ辐射的反应。与野生型菌株相比，突变体在细胞周期的两个阶段通常表现出更高的敏感性。rad50 - 55菌株完全没有出芽期细胞抗性。rad6、9和18突变体表现出一定程度的出芽期细胞抗性。rad2和rec4菌株的反应与相应野生型菌株相同。这些结果表明，与依赖RAD2和RAD6、9和18基因座的途径相比，依赖RAD50 - 55基因座表达的途径在出芽期细胞中功能更有效。姐妹染色单体之间的重组似乎在出芽期细胞抗性中起重要作用，并且这个过程受RAD52修复途径的控制。讨论了与出芽期细胞抗性相关的修复途径和辐照后细胞恢复（LHR）之间的关系。
