Abstract
AbstractIn fungi, ambient pH acts as a key regulator of development and virulence. The vascular wilt pathogenFusarium oxysporumuses host alkalinization to promote infection of plant hosts through activation of the invasive growth mitogen-activated protein kinase (MAPK) Fmk1. The molecular events underlying pH-driven MAPK regulation are unknown. Using the ratiometric GFP-based pH sensor pHluorin, we find that bothF. oxysporumandSaccharomyces cerevisiaerespond to extracellular alkalinization or acidification with a transitory shift in cytosolic pH (pHc) and rapid changes in phosphorylation levels of the three fungal MAPKs Fmk1, Mpk1/Slt2 (cell wall integrity) and Hog1 (hyperosmotic stress). Pharmacological inhibition of the essential plasma membrane H+-ATPase Pma1, which leads to pHcacidification, is sufficient to trigger reprogramming of MAPK phosphorylation even in the absence of an extracellular pH shift. Screening of a subset ofS. cerevisiaemutants identified the sphingolipid-regulated AGC kinase Ypk1/2 as a key upstream component of pHc-modulated MAPK responses. We further show that acidification of pHcinF. oxysporumleads to an increase of the long chain base (LCB) sphingolipid dihydrosphingosine (dhSph) and that exogenous addition of dhSph activates Mpk1 phosphorylation. Our results reveal a pivotal role of pHcin the regulation of MAPK signaling and suggest new ways to control fungal growth and pathogenicity.
Publisher
Cold Spring Harbor Laboratory
Cited by
1 articles.
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