FpNuc1α regulates phosphate signaling and pathogenicity in Fusarium proliferatum infection of jujube fruit by targeting FpGit1 via a novel BSN motif.
TL;DR
These findings uncover a specific regulatory mechnism linking phosphate sensing to the infection process of F. proliferatum, providing potential molecular targets for developing novel fungicides to control postharvest decay and ensure food safety.
Abstract
Fusarium proliferatum is a postharvest pathogen responsible for severe rot in economically important fruits and vegetables, leading to food waste and safety concerns due to mycotoxin contamination. While the PHO signaling pathway is known to regulate phosphate homeostasis, its specific contribution to the virulence mechanisms of this foodborne pathogen remains unclear. In this study, we functionally characterized key components of the PHO pathway in F. proliferatum. Targeted deletion of PHO pathway genes (FpNuc1α, FpNuc1β, FpNuc2, FpPho80, and FpPho85) revealed their essential roles in vegetative growth, conidiation, and stress responses critical for surviving in storage environments. Transcription factor FpNuc1α is required for the full virulence of F. proliferatum. We demonstrate that FpNuc1α activity is tightly controlled by a phosphorylation switch in response to phosphate availability. Furthermore, we discovered that FpNuc1α recognizes a novel DNA motif (BSN) to directly activate FpGit1 gene, a glycerophosphodiester transporter required for full virulence. These findings uncover a specific regulatory mechnism linking phosphate sensing to the infection process of F. proliferatum, providing potential molecular targets for developing novel fungicides to control postharvest decay and ensure food safety.