Article ID Journal Published Year Pages File Type
5504547 Biochemical and Biophysical Research Communications 2017 6 Pages PDF
Abstract

•The transcription factors Ecm22 and Upc2 play a key role in budding yeast mating.•Ecm22 and Upc2 regulate basal and pheromone-induced expression of PRM1 and PRM4.•Deletion of the Ecm22/Upc2 target gene PRM4 results in defective mating.•PRM1 but not PRM4 expression is also regulated by the mating transcription factor Ste12.•Ecm22/Upc2 and Ste12 regulate PRM1 expression through independent pathways.

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.

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