Fus3‐triggered Tec1 degradation modulates mating transcriptional output during the pheromone response

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Abstract
The yeast transcription factor Ste12 controls both mating and filamentation pathways. Upon pheromone induction, the mitogen‐activated protein kinases, Fus3 and Kss1, activate Ste12 by relieving the repression of two functionally redundant Ste12 inhibitors, Dig1 and Dig2. Mating genes are controlled by the Ste12/Dig1/Dig2 complex through Ste12‐binding sites, whereas filamentation genes are regulated by the Tec1/Ste12/Dig1 complex through Tec1‐binding sites. The two Ste12 complexes are mutually exclusive. During pheromone response, Tec1 is degraded upon phosphorylation by Fus3, preventing cross‐activation of the filamentation pathway. Here, we show that a stable Tec1 also impairs the induction of mating genes. A mathematical model is developed to capture the dynamic formation of the two Ste12 complexes and their interactions with pathway‐specific promoters. By model simulations and experimentation, we show that excess Tec1 can impair the mating transcriptional output because of its ability to sequester Ste12, and because of a novel function of Dig2 for the transcription of mating genes. We suggest that Fus3‐triggered Tec1 degradation is an important part of the transcriptional induction of mating genes during the pheromone response.