钙调神经磷酸酶反应性转录因子Crz1通过芽殖酵母中CMK2启动子上唯一的钙调磷酸酶依赖性反应元件（CDRE）位点来调节CMK2的表达。

The calcineurin-responsive transcription factor Crz1 regulates the expression of CMK2 via a sole CDRE site in its promoter in budding yeast.

作者信息

Jiang Linghuo, Gu Yiying, Jiang Yongqiang, Wei Liudan, Meng Lijun, Guan Ni

机构信息

Laboratory of Yeast Biology and Ethanol Fermentation Technology, State Key Laboratory of Non-Food Biomass Energy Technology, Institute of Biological Sciences and Technology, National Engineering Research Center for Non-Food Biorefinery, Guangxi Biomass Engineering Technology Research Center, Guangxi Academy of Sciences, Nanning, 530007, Guangxi, China.

Institute of Biology, Guangxi Academy of Sciences, Nanning, 530007, Guangxi, China.

出版信息

Sci Rep. 2025 Feb 27;15(1):7046. doi: 10.1038/s41598-025-91599-4.

DOI:10.1038/s41598-025-91599-4

PMID:40016385

原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11868491/

Abstract

As a yeast homolog of mammalian calcium/calmodulin-dependent protein kinase II (CaMKII), Cmk2 functions as a negative regulator of calcium signaling in Saccharomyces cerevisiae. We show here that the transcription expression of CMK2 is controlled mainly by the transcription factor Crz1 and also by other factor(s) in response to calcium stress. There are four potential binding sites (calcium/calcineurin-dependent responsive elements; CDREs) for Crz1 in the promoter of CMK2. Through mutational analysis, we demonstrated that mutation of only the site (5' GAGGCT 3'), but not the other three sites, abolished the calcium-induction activity of the CMK2p-lacZ reporter. EMSA analysis indicated that the C-terminal region of Crz1, which contains its DNA-binding domains can bind to this site in vitro. ChIP analysis revealed that Crz1 binds to the promoter region containing this site in vivo. Therefore, the transcription expression of CMK2 is controlled by Crz1 through a sole CDRE site the CMK2 promoter.

摘要

作为哺乳动物钙/钙调蛋白依赖性蛋白激酶II（CaMKII）的酵母同源物，Cmk2在酿酒酵母中作为钙信号的负调节因子发挥作用。我们在此表明，CMK2的转录表达主要受转录因子Crz1控制，也受其他因子响应钙应激的调控。CMK2启动子中有四个Crz1的潜在结合位点（钙/钙调神经磷酸酶依赖性反应元件；CDREs）。通过突变分析，我们证明仅该位点（5' GAGGCT 3'）的突变，而非其他三个位点的突变，消除了CMK2p-lacZ报告基因的钙诱导活性。电泳迁移率变动分析表明，Crz1包含其DNA结合结构域的C末端区域在体外可与该位点结合。染色质免疫沉淀分析显示，Crz1在体内与包含该位点的启动子区域结合。因此，CMK2的转录表达由Crz1通过CMK2启动子中的唯一CDRE位点控制。