Genetic control of repair of radiation damage produced under euoxic and anoxic conditions in diploid yeastSaccharomyces cerevisiae
Genetic control of repair of radiation damage produced under euoxic and anoxic conditions in diploid yeastSaccharomyces cerevisiae
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二倍体酿酒酵母在好氧和缺氧条件下辐射损伤修复的遗传控制
DOI：
10.1007/bf01324186
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发表时间：
1981
影响因子：
1.7
通讯作者：
B. Rao
中科院分区：
文献类型：
--
作者：
N. Reddy;B. Rao
本研究以二倍体野生型酵母菌株211、X2180和辐射敏感突变株rad 2、6、9、18、50-55和57为材料，在有氧和无氧条件下，进行60-Co γ射线照射，以鉴定参与亚致死损伤修复（SLD）、潜在致死损伤恢复（PLD）和氧增强比（OER）的RAD基因座。根据存活曲线参数Dq、D10、D1和D 0比较野生型和突变体的反应。与野生型相比，突变体表现出增加的敏感性辐射致死，无论是在缺氧和缺氧条件下，判断减少Dq和D 0值。OER在突变体2、9、18、50、51和57中降低，表明这些基因可能与低氧条件下γ辐射损伤的修复有关。肩（Dq）是细胞修复SLD的能力的量度，在突变体6、9、18、50、53和57中降低，而在突变体51、52、54、56和57中几乎不存在。突变体55个。2、6、9、18株菌恢复力与野生型相当，53、55、57株菌恢复力较弱，50 -52、54株菌恢复力不强。在具有持液恢复能力的突变体中，从在常氧和低氧条件下产生的PLD中恢复的程度是相同的。这些观察结果表明，不同的基因座组参与了不同修复过程的控制，并且therad 50- 57个位点在电离辐射损伤的修复中起着非常重要的作用。根据本文提供的液体保持恢复数据和其他人的观察，我们认为未修复的DSB构成了PLD，DSB的修复涉及DSB之间的重组。同源染色体
SummaryDiploid wild type yeast strains 211, X2180 and the radiation sensitive mutantsrad2, 6, 9, 18, 50–55, and57 were exposed to cobalt-60 gamma radiation, in the presence and absence of oxygen, in order to identify the RAD loci involved in the repair of sublethal damage (SLD), recovery from potentially lethal damage (PLD) and oxygen enhancement ratio (OER). Response of wild type and mutants were compared in terms of survival curve parameters Dq, D10, D1, and D0. As compared to wild type the mutants showed increased sensitivity to radiation lethality, both under euoxic and hypoxic conditions, as judged by the reduction in Dq and D0 values. OER was reduced in therad2, 9, 18, 50, 51, and57 mutants indicating that these genes could be associated with the repair of gamma radiation damage produced under hypoxic condition.Shoulder (Dq) a measure of the ability of the cells to repair SLD, was reduced in therad6, 9, 18, 50, 53, and57 strains and was almost absent in therad51, 52, 54, and55 mutants. The ability to recover from PLD was equal to that of wild type strain in therad2, 6, 9, and18 strains, reduced in therad53, 55, and57 strains and was absent in therad50–52 and54 strains. In the mutants with liquid holding recovery ability, the extent of recovery from PLD produced under euoxic and hypoxic conditions was the same. These observations suggest that different groups of loci are involved in the control of different repair processes and that the expression of therad50–57 loci play a very important role in the repair of ionising radiation damage.On the basis of the liquid holding recovery data presented here and the observations made by others it is suggested that the unrepaired DSB constitute the PLD and that the repair of DSB involves recombination between homologous chromosomes.