Mutoh Norihiro, Nakagawa Chiaki W, Yamada Kenichiro
Department of Genetics, Institute for Developmental Research, Aichi Human Service Center, Kagiya-cho, Kasugai, Aichi 480-0392, Japan.
Curr Genet. 2002 May;41(2):82-8. doi: 10.1007/s00294-002-0288-9. Epub 2002 Apr 19.
A Cu, Zn-superoxide dismutase gene ( sod1+) deletion mutant of fission yeast Schizosaccharomyces pombe was constructed and its properties were investigated. Superoxide dismutase activity was not detected in the mutant on activity staining of polyacrylamide gels. The mutant showed cysteine or methionine and lysine auxotrophy, slow growth and sensitivity to menadione. While expression of the apt1+ gene, induction of which depends on the Pap1 transcription factor, was induced at the same concentration of menadione in both the wild-type cell and the sod1 mutant, expression of the gpx1+ gene, induction of which depends on the Atf1 transcription factor, was induced at a lower concentration of menadione in the mutant compared with the wild-type control. Expression of the sod1+ gene was induced by oxidative stress and no induction was observed in pap1, prr1 and spc1 mutants.
构建了粟酒裂殖酵母(Schizosaccharomyces pombe)的一个铜锌超氧化物歧化酶基因(sod1+)缺失突变体,并对其特性进行了研究。在聚丙烯酰胺凝胶活性染色中未在该突变体中检测到超氧化物歧化酶活性。该突变体表现出半胱氨酸或甲硫氨酸以及赖氨酸营养缺陷型、生长缓慢和对甲萘醌敏感。虽然依赖于Pap1转录因子诱导的apt1+基因在野生型细胞和sod1突变体中在相同浓度的甲萘醌下均被诱导,但依赖于Atf1转录因子诱导的gpx1+基因在突变体中比野生型对照在更低浓度的甲萘醌下被诱导。sod1+基因的表达由氧化应激诱导,而在pap1、prr1和spc1突变体中未观察到诱导现象。