Mach K E, Cheng Q, Albright C F
655 Light Hall, Vanderbilt University School of Medicine, Nashville, TN 37232-0146, USA.
Curr Genet. 1998 Sep;34(3):172-82. doi: 10.1007/s002940050383.
To identify novel components of ras1+ signalling in Schizosaccharomyces pombe, extragenic suppressors of the mating defect of ras1 effector mutants were isolated. A novel allele of pat1, pat1-e1, was isolated that increases the mating of ras1-D43E mutants to near wild-type levels but does not suppress the mating defect of ras1-I41M, ras1-Y37F, or ras1-Y45I mutants. This allele-specific suppression is not a characteristic of all pat1 alleles since pat1-3 and pat1-114 partially and equally suppress ras1-D43E and ras1-I41M mutants. Analysis of mating cultures showed that ras1-D43E and pat1-e1 interact to qualitatively alter the mating response. While pat1-e1 ras1-D43E cells were delayed in agglutination, cell-cycle delay, and mat1-Pm transcription, they induce mat1-Mc at the same time and mate more rapidly than other mating cultures. These results suggest that pheromone signalling, but not nutritional signalling, is delayed in pat1-e1 ras1-D43E cells. We hypothesize that this delay causes an elevated pheromone response and thus suppression of the mating defect of the ras1-D43E mutant by pat1-e1.
为了鉴定粟酒裂殖酵母中ras1+信号传导的新组分,我们分离了ras1效应突变体交配缺陷的基因外抑制子。分离出了pat1的一个新等位基因pat1-e1,它能将ras1-D43E突变体的交配能力提高到接近野生型水平,但不能抑制ras1-I41M、ras1-Y37F或ras1-Y45I突变体的交配缺陷。这种等位基因特异性抑制并非所有pat1等位基因的特征,因为pat1-3和pat1-114能部分且同等程度地抑制ras1-D43E和ras1-I41M突变体。对交配培养物的分析表明,ras1-D43E和pat1-e1相互作用,在质量上改变了交配反应。虽然pat1-e1 ras1-D43E细胞在凝集、细胞周期延迟和mat1-Pm转录方面有所延迟,但它们同时诱导mat1-Mc,并且比其他交配培养物交配得更快。这些结果表明,在pat1-e1 ras1-D43E细胞中,信息素信号传导而非营养信号传导被延迟。我们推测,这种延迟导致信息素反应增强,从而pat1-e1抑制了ras1-D43E突变体的交配缺陷。