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对交配激素α-因子导致的G1期阻滞超敏感的酿酒酵母突变体的分离与鉴定

Isolation and characterization of Saccharomyces cerevisiae mutants supersensitive to G1 arrest by the mating hormone a-factor.

作者信息

Steden M, Betz R, Duntze W

机构信息

Institut für Physiologische Chemie, Ruhr-Universität Bochum, Federal Republic of Germany.

出版信息

Mol Gen Genet. 1989 Nov;219(3):439-44. doi: 10.1007/BF00259617.

Abstract

Nine independent mutants which are supersensitive (ssl-) to G1 arrest by the mating hormone a-factor were isolated by screening mutagenized Saccharomyces cerevisiae MAT alpha cells on solid medium for increased growth inhibition with a-factor. These mutants carried lesions in two complementation groups, ssl1 and ssl2. Mutations at the ssl1 locus were mating type specific: MAT alpha ssl1- cells were supersensitive to a-factor but MATa ssl1- were not supersensitive to alpha-factor. In contrast, mutations at the ssl2 locus conferred supersensitivity to the mating hormone of the opposite mating type on both MAT alpha and MATa cells. The alpha-cell specific capacity to inactivate externally added a-factor was shown to be lacking in MAT alpha ssl1- mutants whereas MAT alpha ssl2- cells were able to inactivate a-factor. Complementation analysis showed that ssl2 and sst2, a mutation originally isolated as conferring supersensitivity to alpha-factor to MATa cells, are lesions in the same gene. The ssl1 gene was mapped 30.5 centiMorgans distal to ilv5 on chromosome XII.

摘要

通过在固体培养基上筛选诱变的酿酒酵母MATα细胞,以检测α因子对生长抑制作用的增强,从而分离出九个对交配激素α因子引起的G1期阻滞超敏感(ssl-)的独立突变体。这些突变体在两个互补群ssl1和ssl2中存在缺陷。ssl1位点的突变具有交配型特异性:MATα ssl1-细胞对α因子超敏感,但MATa ssl1-细胞对α因子不超敏感。相反,ssl2位点的突变使MATα和MATa细胞对相反交配型的交配激素都表现出超敏感性。已证明MATα ssl1-突变体缺乏α细胞特异性的使外源添加的α因子失活的能力,而MATα ssl2-细胞能够使α因子失活。互补分析表明,ssl2和sst2(最初分离出的一种使MATa细胞对α因子超敏感的突变)是同一基因中的缺陷。ssl1基因定位于第十二号染色体上ilv5远端30.5厘摩处。

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