...
  • 主题
高级搜索  >
历史搜索 清空历史
首页> 外文期刊>Molecular and Cellular Biology >The yeast ARD1 gene product is required for repression of cryptic mating-type information at the HML locus.
【24h】

The yeast ARD1 gene product is required for repression of cryptic mating-type information at the HML locus.

机译：酵母ARD1基因产物是抑制HML位点隐性交配型信息所必需的。

获取原文
           
页面导航
  • 摘要
  • 著录项
  • 相似文献
  • 相关主题

摘要

Mutations in the ARD1 gene prevent yeast cells from displaying G1-specific growth arrest in response to nitrogen deprivation and cause MATa haploids (but not MAT alpha haploids) to be mating defective. Analysis of cell type-specific gene expression by examination of RNA transcripts and measurement of beta-galactosidase activity from yeast gene-lacZ fusions demonstrated that the mating defect of MATa ard1 mutants was due to an inability to express genes required by MATa cells for the mating process. The lack of mating-specific gene expression in MATa cells was found to be due solely to derepression of the normally silent alpha information at the HML locus. The cryptic a information at the HMR locus was only very slightly derepressed in ard1 mutants, to a level insufficient to affect the mating efficiency of MAT alpha cells. The preferential elevation of expression from HML over HMR was also observed in ard1 mutants which contained the alternate arrangement of a information at HML and alpha information at HMR. Hence, the effect of the ard1 mutation was position specific (rather than information specific). Although the phenotype of ard1 mutants resembled that of cells with mutations in the SIR1 gene, both genetic and biochemical findings indicated that ARD1 control of HML expression was independent of the regulation imposed by SIR1 and the other SIR genes. These results suggest that the ARD1 gene encodes a protein product that acts, directly or indirectly, at the HML locus to repress its expression and, by analogy, may control expression of other genes involved in monitoring nutritional conditions.
机译：ARD1基因的突变阻止酵母细胞响应氮剥夺而显示G1特异性生长停滞，并导致MATa单倍体（但不是MATα单倍体）交配缺陷。通过检查RNA转录本和测量酵母基因-lacZ融合蛋白的β-半乳糖苷酶活性来分析细胞类型特异性基因表达，这表明MATa ard1突变体的交配缺陷是由于无法表达MATa细胞交配所需的基因处理。发现在MATa细胞中缺乏交配特异性基因表达仅是由于HML基因座上通常沉默的α信息的抑制所致。在ard1突变体中，HMR基因座处的信息a隐含的抑制非常轻微，不足以影响MAT alpha细胞的交配效率。在ard1突变体中也观察到HML相对于HMR优先表达，该突变体包含HML信息和HMRα信息的交替排列。因此，ard1突变的影响是位置特定的（而不是信息特定的）。尽管ard1突变体的表型与SIR1基因中具有突变的细胞的表型相似，但是遗传和生化发现均表明ARD1对HML表达的控制独立于SIR1和其他SIR基因的调控。这些结果表明，ARD1基因编码一种蛋白质产物，该蛋白质产物直接或间接在HML位点发挥作用，以抑制其表达，并且类似地，可以控制参与监测营养状况的其他基因的表达。

著录项

相似文献

  • 外文文献
  • 中文文献
  • 专利
获取原文

客服邮箱：kefu@zhangqiaokeyan.com

京公网安备：11010802029741号 ICP备案号：京ICP备15016152号-6 六维联合信息科技 (北京) 有限公司©版权所有

  • 客服微信

  • 服务号