Kato T, Okazaki K, Murakami H, Stettler S, Fantes P A, Okayama H
Okayama Cell Switching Project, ERATO, JRDC, Kyoto, Japan.
FEBS Lett. 1996 Jan 15;378(3):207-12. doi: 10.1016/0014-5793(95)01442-x.
We identified the phh1+ gene that encodes a MAP kinase as the effector of Wis1 MAP kinase kinase in fission yeast, which is highly homologous with HOG1 of S. cerevisiae. Heterothalic phh1 dsiruptant is phenotypically indistinguishable from wis1 deletion mutant, both displaying the same extent of partial sterility and enhanced sensitivity to a variety of stress. In phh1 disruptant, nitrogen starvation-induced expression of ste11+, a key controller of sexual differentiation, is markedly diminished. Ectopic expression of ste11+ effectively restores fertility, but not stress resistance, to the phh1 disruptant. These data show that stress signal, mediated by a MAP kinase, is required for efficient start of sexual differentiation.
我们鉴定出编码一种丝裂原活化蛋白激酶(MAP激酶)的phh1+基因,它是裂殖酵母中Wis1 MAP激酶激酶的效应物,与酿酒酵母的HOG1高度同源。异宗配合的phh1缺失突变体在表型上与wis1缺失突变体无法区分,二者都表现出相同程度的部分不育以及对多种胁迫的敏感性增强。在phh1缺失突变体中,氮饥饿诱导的性分化关键调控因子ste11+的表达显著降低。ste11+的异位表达有效地恢复了phh1缺失突变体的育性,但未恢复其抗胁迫能力。这些数据表明,由MAP激酶介导的胁迫信号是性分化有效启动所必需的。