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对α-因子超敏感的MATa细胞中MFα1的表达导致自我停滞。

Expression of MF alpha 1 in MATa cells supersensitive to alpha-factor leads to self-arrest.

作者信息

Whiteway M, Hougan L, Thomas D Y

机构信息

Genetic Engineering Section, NRC Biotechnology Research Institute, Montreal, Que., Canada.

出版信息

Mol Gen Genet. 1988 Sep;214(1):85-8. doi: 10.1007/BF00340184.

Abstract

MATa cells of Saccharomyces cerevisiae defective in both the SST1 and SST2 gene products exhibit self-arrest when they express the MF alpha 1 gene under the control of the GAL1 promoter. This response to endogenously produced pheromone can be alleviated by mutations which prevent the production of, or response to, alpha-factor. Suppressors of the self-arrest phenotype include a class of mutants which remain responsive to low levels of pheromone, but are resistant to high levels of alpha-factor. One of these mutants has been mapped to chromosome X, 31 cM distal to SUP4, and defines a new locus designated STE18.

摘要

在SST1和SST2基因产物均有缺陷的酿酒酵母MATa细胞,当它们在GAL1启动子控制下表达MFα1基因时会出现自我停滞。这种对内源性产生的信息素的反应可以通过阻止α因子产生或对其反应的突变来缓解。自我停滞表型的抑制子包括一类突变体,它们对低水平的信息素仍有反应,但对高水平的α因子具有抗性。其中一个突变体已被定位到X染色体上,位于SUP4远端31厘摩处,并定义了一个新的基因座,命名为STE18。

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