PSO4 - A NOVEL GENE INVOLVED IN ERROR-PRONE REPAIR IN SACCHAROMYCES-CEREVISIAE
PSO4 - A NOVEL GENE INVOLVED IN ERROR-PRONE REPAIR IN SACCHAROMYCES-CEREVISIAE
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DOI：
10.1016/0921-8777(89)90017-7
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发表时间：
1989-09-01
期刊：
影响因子：
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通讯作者：
SCHENBERG, ACG
中科院分区：
文献类型：
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作者：
HENRIQUES, JAP;VICENTE, EJ;SCHENBERG, ACG
单倍体xs9突变体最初是基于对X射线的致死效应的轻微敏感性而选择的，被发现对8-甲氧补骨脂素(8MOP)的光加成非常敏感，特别是当细胞处于细胞周期的G2期时。由于xs9突变与已知的3个PSO突变中的任何一个都没有等位基因，它现在被命名为pso4-1。在失活方面，突变体pso4-1对单(HN1)或双功能(HN2)氮素也敏感，对254 nm紫外光(UV)略敏感，对3-甲氧补骨脂素(3-CPS)光加成或甲烷磺酸甲酯(MMS)表现出接近正常的敏感性。在诱变方面，pso4-1突变完全阻止了8MOP或3CPs光加成或伽马射线诱导的反向和正向突变。在UV、HN1、HN2或MMS处理的情况下，虽然回复诱导仍然完全取消，但对UV、HN1或MMS的正向突变只被部分抑制，而对HN2不受影响。除了严重抑制诱变作用外，pSO4-1突变还表现为半显性突变，抑制产孢量，消除二倍体抗性效应，阻断诱导的有丝分裂重组，这表明PSO4基因参与了一条易于错误修复的重组途径，类似于大肠杆菌的SOS修复途径。
The haploid xs9 mutant, originally selected for on the basis of the slight sensitivity to the lethal effect of X-rays, was found to be extremely sensitive to inactivation by 8-methoxypsoralen (8MOP) photoaddition, especially when cells are treated in the G2 phase of the cell cycle. As the xs9 mutation showed no allelism with any of the 3 known pso mutations, it was now given the name of pso4-1. Regarding inactivation, the pso4-1 mutant is also sensitive to mono-(HN1) or bi-functional (HN2) nitrogen mustards, it is slightly sensitive to 254 nm UV radiation (UV), and shows nearly normal sensitivity to 3-carbethoxypsoralen (3-CPs) photoaddition or methyl methanesulfonate (MMS). Regarding mutagenesis, the pso4-1 mutation completely blocks reverse and forward mutations induced by either 8MOP or 3CPs photoaddition, or by .gamma.-rays. In the cases of UV, HN1, HN2, or MMS treatments, while reversion induction is still completely abolished, forward mutagenesis is only partially inhibited for UV, HN1, or MMS, and it is unaffected for HN2. Besides severely inhibiting induced mutagenesis, the pso4-1 mutation was found to be semi-dominant, to block sporulation, to abolish the diploid resistance effect, and to block induced mitotic recombination, which indicates that the PSO4 gene is involved in a recombinational pathway of error-prone repair, comparable to the E. coli SOS repair pathway.