Investigating the role of phosphodiesterase Pde2 in coordinating resource reallocation through the environmental stress response.
TL;DR
Investigating the role of the upstream regulator Pde2 in ESR regulation and poststress fitness found pde2Δ cells had normal or faster poststress growth rates, despite weaker activation of the ESR.
Abstract
Yeast responding to acute stress reallocates cellular resources, in part via the environmental stress response (ESR) that induces stress-defense genes while repressing ribosome biogenesis and growth genes. The purpose and regulation of coordinated induction and repression are incompletely understood, but both responses are influenced by ESR transcription factors Msn2 and Msn4 (Msn2/4). Here, we used single-cell microscopy and transcriptomic analysis to investigate the role of the upstream regulator Pde2 in ESR regulation and poststress fitness. Loss of PDE2 weakened and shortened Msn2 activation following salt stress and produced muted induction of Msn2/4 targets, similar to a msn2Δmsn4Δ strain. In contrast, Pde2 had at most a minor impact on the ESR repressor Dot6, yet was important for repression of its targets beyond Msn2/4 influence. Consistent with our recent resource-reallocation model, pde2Δ cells had normal or faster poststress growth rates, despite weaker activation of the ESR. We discuss implications for ESR regulation and function.