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酿酒酵母中蛋白酶B结构基因PRB1的调控

Regulation of the proteinase B structural gene PRB1 in Saccharomyces cerevisiae.

作者信息

Naik R R, Nebes V, Jones E W

机构信息

Department of Biological Sciences, Mellon Institute, Carnegie Mellon University, Pittsburgh, Pennsylvania 15213, USA.

出版信息

J Bacteriol. 1997 Mar;179(5):1469-74. doi: 10.1128/jb.179.5.1469-1474.1997.

Abstract

The expression of PRB1, the gene that encodes the precursor to the soluble vacuolar proteinase B (PrB) in Saccharomyces cerevisiae, is regulated by carbon and nitrogen sources and by growth phase. Little or no PRB1 mRNA is detectable during exponential growth on glucose as the carbon source; it begins to accumulate as cells exhaust the glucose. Previous work has shown that glucose repression of PRB1 transcription is not mediated by HXK2 or by the SNF1, SNF4, and SNF6 genes (C. M. Moehle and E. W. Jones, Genetics 124:39-55, 1990). We analyzed the effects of mutations in the MIG1, TUP1, and GRR1 genes on glucose repression of PRB1 and found that mutations in each partially alleviate glucose repression. tup1 and mig1 mutants fail to translocate all of the Prb1p into the lumen of the endoplasmic reticulum. A screen for new mutants revealed mutations in MIG1 and REG1, genes already known to regulate glucose repression, as well as in three new genes that we have named PBD1 to PBD3; all cause derepressed expression. Mutations that result in failure to completely derepress PRB1 were also identified in two new genes, named PND1 and PND2. Good nitrogen sources, like ammonia, repress PRB1 transcription; mutations in URE2 do not affect this response. Derepression upon transfer to a poor nitrogen source is dependent upon GLN3.

摘要

PRB1基因编码酿酒酵母中可溶性液泡蛋白酶B(PrB)的前体,其表达受碳源、氮源和生长阶段的调控。在以葡萄糖作为碳源的指数生长期,几乎检测不到PRB1 mRNA;当细胞耗尽葡萄糖时,它开始积累。先前的研究表明,PRB1转录的葡萄糖抑制作用不是由HXK2或SNF1、SNF4和SNF6基因介导的(C.M. Moehle和E.W. Jones,《遗传学》124:39 - 55,1990)。我们分析了MIG1、TUP1和GRR1基因的突变对PRB1葡萄糖抑制作用的影响,发现每个基因的突变都部分缓解了葡萄糖抑制作用。tup1和mig1突变体无法将所有Prb1p转运到内质网腔中。对新突变体的筛选揭示了MIG1和REG1基因(已知调控葡萄糖抑制作用)以及我们命名为PBD1至PBD3的三个新基因中的突变;所有这些突变都导致去抑制表达。在两个名为PND1和PND2的新基因中也鉴定出了导致PRB1不能完全去抑制的突变。良好的氮源,如氨,会抑制PRB1转录;URE2基因的突变不影响这种反应。转移到劣质氮源后去抑制作用依赖于GLN3。

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