Osmotic balance regulates cell fusion during mating in Saccharomyces cerevisiae.
Osmotic balance regulates cell fusion during mating in Saccharomyces cerevisiae.
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DOI：
10.1083/jcb.138.5.961
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发表时间：
1997-09-08
影响因子：
7.8
通讯作者：
Herskowitz, I
中科院分区：
文献类型：
--
作者：
Philips, J;Herskowitz, I
酵母交配过程中合子的成功形成需要两个单倍体交配伙伴的细胞融合。为了确保细胞在重塑细胞壁时不会溶解，融合事件在时间和空间上都是受调控的：只有在细胞-细胞接触后，细胞壁才会降解，而且只在细胞-细胞接触的区域。为了了解细胞融合是如何受到调控的，我们根据它们与FUS1融合2菌株(Chenevert，J.，N.Valtz和I.Herskowitz)交配的缺陷，确定了细胞融合中存在缺陷的突变体。1994年。遗传学136：1287-1297)。这些细胞融合突变体中有两个在FPS1基因上存在缺陷，该基因编码甘油促进剂(Luyten，K.，J.Albertyn，W.F.Skibbe，B.A.Prior，J.Ramos，J.M.Thevelein和S.Hohmann)。1995年。EMBO[欧元摩尔。比奥尔。器官。]J.14：1360-1371)。为了确定无法维持渗透平衡是否导致这些突变体中细胞融合的缺陷，我们分析了由于甘油-3-磷酸脱氢酶(GPD1)基因缺陷而导致细胞内甘油水平降低的fps 1Δ突变体的行为(Albertyn，J.，S.Hohmann，J.M.Thevelein和B.A.Prior)。1994年。摩尔。牢房。比奥尔。14：4135-4144)：GPD1的缺失部分抑制了fps1突变体的细胞融合缺陷。相反，GPD1的过表达加剧了这种缺陷。1M山梨醇也能部分抑制融合缺陷。这些观察表明，fps1突变体的融合缺陷是由于无法调节渗透平衡，并提供了细胞渗透状态可以调节融合的证据。我们还观察到，表达高活性蛋白激酶C的突变体表现出与fps1突变体相似的细胞融合缺陷。我们认为Pkc1p调节细胞融合以响应渗透不平衡。与fps1突变体不同，Fus1和fus2突变体不受GPD1表达或1M山梨醇的影响。因此，它们的融合缺陷不太可能是渗透平衡改变造成的。
Successful zygote formation during yeast mating requires cell fusion of the two haploid mating partners. To ensure that cells do not lyse as they remodel their cell wall, the fusion event is both temporally and spatially regulated: the cell wall is degraded only after cell–cell contact and only in the region of cell–cell contact. To understand how cell fusion is regulated, we identified mutants defective in cell fusion based upon their defect in mating to a fus1 fus2 strain (Chenevert, J., N. Valtz, and I. Herskowitz. 1994. Genetics 136:1287–1297). Two of these cell fusion mutants are defective in the FPS1 gene, which codes for a glycerol facilitator (Luyten, K., J. Albertyn, W.F. Skibbe, B.A. Prior, J. Ramos, J.M. Thevelein, and S. Hohmann. 1995. EMBO [Eur. Mol. Biol. Organ.] J. 14:1360–1371). To determine whether inability to maintain osmotic balance accounts for the defect in cell fusion in these mutants, we analyzed the behavior of an fps1Δ mutant with reduced intracellular glycerol levels because of a defect in the glycerol-3-phosphate dehydrogenase (GPD1) gene (Albertyn, J., S. Hohmann, J.M. Thevelein, and B.A. Prior. 1994. Mol. Cell. Biol. 14:4135– 4144): deletion of GPD1 partially suppressed the cell fusion defect of fps1 mutants. In contrast, overexpression of GPD1 exacerbated the defect. The fusion defect could also be partially suppressed by 1 M sorbitol. These observations indicate that the fusion defect of fps1 mutants results from inability to regulate osmotic balance and provide evidence that the osmotic state of the cell can regulate fusion. We have also observed that mutants expressing hyperactive protein kinase C exhibit a cell fusion defect similar to that of fps1 mutants. We propose that Pkc1p regulates cell fusion in response to osmotic disequilibrium. Unlike fps1 mutants, fus1 and fus2 mutants are not influenced by expression of GPD1 or by 1 M sorbitol. Their fusion defect is thus unlikely to result from altered osmotic balance.
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64.5
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