THE YEAST ARD1 GENE-PRODUCT IS REQUIRED FOR REPRESSION OF CRYPTIC MATING-TYPE INFORMATION AT THE HML LOCUS
THE YEAST ARD1 GENE-PRODUCT IS REQUIRED FOR REPRESSION OF CRYPTIC MATING-TYPE INFORMATION AT THE HML LOCUS
复制标题
DOI：
10.1128/mcb.7.10.3713
复制
发表时间：
1987-10-01
影响因子：
5.3
通讯作者：
THORNER, J
中科院分区：
文献类型：
--
作者：
WHITEWAY, M;FREEDMAN, R;THORNER, J
ARD1 基因突变会阻止酵母细胞响应氮缺乏而表现出 G1 特异性生长停滞，并导致 MATa 单倍体（但不是 MAT.α. 单倍体）出现交配缺陷。通过检查RNA转录本和测量来自酵母基因-lacZ融合体的β-半乳糖苷酶活性来分析细胞类型特异性基因表达，证明MATa ard1突变体的交配缺陷是由于无法表达MATa细胞交配过程所需的基因。发现 MATa 细胞中缺乏交配特异性基因表达仅仅是由于通常沉默的 α 的去抑制。 HML 轨迹的信息。 HMR 位点上的隐含信息在 ard1 突变体中仅受到非常轻微的去抑制，其水平不足以影响 MAT.alpha 的交配效率。细胞。在 ard1 突变体中也观察到 HML 相对于 HMR 的表达优先升高，该突变体包含 HML 和 α 信息的交替排列。 HMR 上的信息。因此，ard1 突变的影响是位置特异性的（而不是信息特异性的）。尽管 ard1 突变体的表型与 SIR1 基因突变的细胞相似，但遗传和生化研究结果表明 ARD1 对 HML 表达的控制独立于 SIR1 和其他 SIR 基因施加的调节。这些结果表明，ARD1 基因编码的蛋白质产物直接或间接作用于 HML 基因座以抑制其表达，并且通过类推，可以控制参与监测营养状况的其他基因的表达。
Mutations in the ARD1 gene prevent yeast cells for 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 mutant 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.