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Ecm22和Upc2通过控制交配基因PRM1和PRM4的表达来调节酵母交配。

Ecm22 and Upc2 regulate yeast mating through control of expression of the mating genes PRM1 and PRM4.

作者信息

Höfken Thomas

机构信息

Division of Biosciences, Brunel University London, Uxbridge, UB8 3PH, UK.

出版信息

Biochem Biophys Res Commun. 2017 Dec 2;493(4):1485-1490. doi: 10.1016/j.bbrc.2017.10.005. Epub 2017 Oct 3.

Abstract

Budding yeast mating is an excellent model for receptor-activated cell differentiation. Here we identify the related transcription factors Ecm22 and Upc2 as novel regulators of mating. Cells lacking both ECM22 and UPC2 display strong mating defects whereas deletion of either gene has no effect. Ecm22 and Upc2 positively regulate basal expression of PRM1 and PRM4. These genes are strongly induced in response to mating pheromone, which is also largely dependent on ECM22 and UPC2. We further show that deletion of PRM4 like PRM1 results in markedly reduced mating efficiency. Expression of PRM1 but not of PRM4 is also regulated by Ste12, a key transcription factor for mating. STE12 deletion lowers basal PRM1 expression, whereas STE12 overexpression strongly increases PRM1 levels. This regulation of PRM1 transcription is mediated through three Ste12-binding sites in the PRM1 promoter. Simultaneous deletion of ECM22 and UPC2 as well as mutation of the three Ste12-binding sites in the PRM1 promoter completely abolishes basal and pheromone-induced PRM1 expression, indicating that Ste12 and Ecm22/Upc2 control PRM1 transcription through distinct pathways. In summary, we propose a novel mechanism for budding yeast mating. We suggest that Ecm22 and Upc2 regulate mating through the induction of the mating genes PRM1 and PRM4.

摘要

出芽酵母的交配是受体激活细胞分化的一个优秀模型。在这里,我们确定相关转录因子Ecm22和Upc2是交配的新型调节因子。同时缺失ECM22和UPC2的细胞表现出强烈的交配缺陷,而单独缺失任何一个基因都没有影响。Ecm22和Upc2正向调节PRM1和PRM4的基础表达。这些基因在交配信息素的作用下被强烈诱导,这在很大程度上也依赖于ECM22和UPC2。我们进一步表明,与PRM1一样,缺失PRM4会导致交配效率显著降低。PRM1的表达受交配关键转录因子Ste12的调节,而PRM4的表达不受其调节。缺失STE12会降低PRM1的基础表达,而STE12的过表达则会强烈提高PRM1的水平。PRM1转录的这种调节是通过PRM1启动子中的三个Ste12结合位点介导的。同时缺失ECM22和UPC2以及PRM1启动子中三个Ste12结合位点的突变完全消除了基础和信息素诱导的PRM1表达,表明Ste12和Ecm22/Upc2通过不同途径控制PRM1转录。总之,我们提出了一种出芽酵母交配的新机制。我们认为Ecm22和Upc2通过诱导交配基因PRM1和PRM4来调节交配。

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