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首页> 外文期刊>Molecular and Cellular Biology >The E2 Ubiquitin Conjugase Rad6 Is Required for the ArgR/Mcm1 Repression of ARG1 Transcription
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The E2 Ubiquitin Conjugase Rad6 Is Required for the ArgR/Mcm1 Repression of ARG1 Transcription

机译：E2泛素结合酶Rad6是ARG1转录的ArgR / Mcm1抑制所必需的。

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Transcription of the Saccharomyces cerevisiae ARG1 gene is under the control of both positive and negative elements. Activation of the gene in minimal medium is induced by Gcn4. Repression occurs in the presence of arginine and requires the ArgR/Mcm1 complex that binds to two upstream arginine control (ARC) elements. With the recent finding that the E2 ubiquitin conjugase Rad6 modifies histone H2B, we examined the role of Rad6 in the regulation of ARG1 transcription. We find that Rad6 is required for repression of ARG1 in rich medium, with expression increased ～10-fold in a rad6 null background. Chromatin immunoprecipitation analysis indicates increased binding of TATA-binding protein in the absence of Rad6. The active-site cysteine of Rad6 is required for repression, implicating ubiquitination in the process. The effects of Rad6 at ARG1 involve two components. In one of these, histone H2B is the likely target for ubiquitination by Rad6, since a strain expressing histone H2B with the principal ubiquitination site converted from lysine to arginine shows a fivefold relief of repression. The second component requires Ubr1 and thus likely the pathway of N-end rule degradation. Through the analysis of promoter constructs with ARC deleted and an arg80 rad6 double mutant, we show that Rad6 repression is mediated through the ArgR/Mcm1 complex. In addition, analysis of an ada2 rad6 deletion strain indicated that the SAGA acetyltransferase complex and Rad6 act in the same pathway to repress ARG1 in rich medium.
机译：酿酒酵母ARG1 基因的转录受正负两个因素的控制。该基因在基本培养基中的激活是由Gcn4诱导的。抑制作用是在精氨酸存在下发生的，需要结合两个上游精氨酸控制（ARC）元素的ArgR / Mcm1复合物。最近发现E2泛素结合酶Rad6修饰了组蛋白H2B，我们研究了Rad6在 ARG1 转录调控中的作用。我们发现Rad6是在丰富培养基中抑制 ARG1 所必需的，在 rad6 空背景下表达增加了约10倍。染色质免疫沉淀分析表明在不存在Rad6的情况下TATA结合蛋白的结合增加。 Rad6的活性位点半胱氨酸是抑制所必需的，这意味着该过程中泛素化。 Rad6对 ARG1 的作用涉及两个部分。在其中一种中，组蛋白H2B可能是Rad6泛素化的靶标，因为表达组蛋白H2B的菌株的主要泛素化位点从赖氨酸转化为精氨酸，其抑制作用减轻了五倍。第二个组件需要Ubr1，因此可能是N端规则降级的途径。通过分析缺失ARC的启动子构建体和 arg80 rad6 双突变体，我们发现Rad6阻遏是通过ArgR / Mcm1复合体介导的。此外，对 ada2 rad6 缺失菌株的分析表明，SAGA乙酰基转移酶复合体和Rad6以相同的途径起作用，以在丰富的培养基中抑制 ARG1 。

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