Paesi-Toresan S O, Pich C T, Grey M, Keszenman-Pereyra D, Brendel M, Henriques J A
Departamento de Biofísica, Universidade Federal do Rio Grando do Sul, Porto Alegre, Brasil.
Curr Genet. 1995 May;27(6):493-5. doi: 10.1007/BF00314437.
The pos5-1 mutation renders Saccharomyces cerevisiae cells sensitive to DNA-damaging agents. We have isolated plasmids from a S. cerevisiae genomic library capable of restoring wild-type levels of 254-nm ultraviolet light sensitivity of the pso5-1 mutant. DNA sequence analysis revealed that the complementing activity resides in RAD16, a gene involved in excision repair. Tetrad analysis showed that PSO5, like RAD16, is tightly linked to LYS2 on chromosome II. Moreover, allelism between the pso5-1 and rad16 mutants was demonstrated by the comparison of mutagen sensitivity phenotypes, complementation tests, and by meiotic analysis. The cloned RAD16 gene was capable of restoring wild-type resistance of the pso5-1 mutant to H2O2 and photoactivated 3-carbethoxypsoralen, both treatments generating oxidative stress-related DNA damage. This indicates that RAD16/PSO5 might also participate in the repair of oxidative base damage.
pos5-1突变使酿酒酵母细胞对DNA损伤剂敏感。我们从酿酒酵母基因组文库中分离出了能够恢复pso5-1突变体对254纳米紫外线敏感性野生型水平的质粒。DNA序列分析表明,互补活性存在于RAD16中,RAD16是一个参与切除修复的基因。四分体分析表明,PSO5与RAD16一样,与II号染色体上的LYS2紧密连锁。此外,通过比较诱变剂敏感性表型、互补试验和减数分裂分析,证明了pso5-1和rad16突变体之间的等位性。克隆的RAD16基因能够恢复pso5-1突变体对H2O2和光活化3-乙氧羰基补骨脂素的野生型抗性,这两种处理都会产生与氧化应激相关的DNA损伤。这表明RAD16/PSO5也可能参与氧化碱基损伤的修复。