A complex regulatory element from the yeast gene ENO2 modulates GCR1-dependent transcriptional activation.

A complex regulatory element from the yeast gene ENO2 modulates GCR1-dependent transcriptional activation.
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来自酵母基因 ENO2 的复杂调控元件可调节 GCR1 依赖性转录激活。

DOI:
10.1128/mcb.13.4.2623-2633.1993
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发表时间:
1993
影响因子:
5.3
通讯作者:
Holland,MJ
Holland,MJ
中科院分区:
生物学2区
文献类型:
--
作者:
Willett,CE;Gelfman,CM;Holland,MJ

文献摘要

相似文献

GCR1基因产物是许多酵母基因(包括编码糖酵解酶的基因)最大程度转录所必需的。在携带 agcr1null 突变的菌株中,酵母烯醇酶基因 ENO2 的转录减少了 50 倍。通过使用通常不依赖于 GCR1 表达的无增强子 CYC1 启动子,鉴定了足以依赖 GCR1 调节 ENO2 表达的顺式作用序列。鉴定出足以提供 CYC1 启动子高水平、GCR1 依赖性转录激活的 60-bpENO2 序列。该 60 bp 元件可细分为包含新 RAP1 结合位点和不激活 CYC1 转录的 GCR1 结合位点的 30 bp 序列,以及包含新增强子元件的 30 bp 序列,该增强子元件可赋予中等水平的不依赖于 GCR1 的转录激活。 60-bpCGCR1 依赖性上游激活剂序列位于先前绘制的调节蛋白 ABFI 和 RAP1 重叠结合位点的紧下游。有证据表明,重叠的 ABFI 和 RAP1 结合位点与结合 GCR1 和 RAP1 的序列一起发挥作用,以实现 ENO2 表达的转录激活。
TheGCR1gene product is required for maximal transcription of many yeast genes including genes encoding glycolytic enzymes. Transcription of the yeast enolase geneENO2is reduced 50-fold in strains carrying agcr1null mutation.cis-acting sequences that are sufficient forGCR1-dependent regulation ofENO2expression were identified by using an enhancerlessCYC1promoter which is not normally dependent onGCR1for expression. A 60-bpENO2sequence that was sufficient to provide high-level,GCR1-dependent transcriptional activation of theCYC1promoter was identified. This 60-bp element could be subdivided into a 30-bp sequence containing a novel RAP1-binding site and a GCR1-binding site which did not activateCYC1transcription and a 30-bp sequence containing a novel enhancer element that conferred moderate levels ofGCR1-independent transcriptional activation. The 60-bpCGCR1-dependent upstream activator sequence is located immediately downstream from previously mapped overlapping binding sites for the regulatory proteins ABFI and RAP1. Evidence is presented that the overlapping ABFI- and RAP1-binding sites function together with sequences that bind GCR1 and RAP1 to stage transcriptional activation ofENO2expression.