FpLaeA Coordinates Fusarium proliferatum Pathogenesis by Orchestrating Mycotoxin Biosynthesis and Host Immune Subversion
TL;DR
It is reported that the methyltransferase FpLaeA is a global regulator essential for F. proliferatum pathogenicity and a target for integrated control of F. proliferatum and its associated mycotoxin risk.
Abstract
Fusarium proliferatum causes rice spikelet rot and contaminates grains with fumonisins. Here, we report that the methyltransferase FpLaeA is a global regulator essential for its pathogenicity. Deletion of FplaeA impaired conidiation and led to conspicuous accumulation of β-1,3-glucan. The ΔFplaeA mutant failed to produce fumonisin B1 (FB1), accompanied by the downregulation of the biosynthetic gene cluster, depletion of the precursor alanine, and disruption of sphingolipid homeostasis. It also showed defective invasive hyphal growth and attenuated secretion of pectate lyase (PL) and polygalacturonase (PG). Crucially, infection by ΔFplaeA triggered an activation of jasmonic acid (JA)-mediated defenses, evidenced by elevated JA levels and upregulated expression of JA biosynthetic genes. Our findings position FpLaeA as a key coordinator of fungal pathogenesis and immune evasion, highlighting its potential as a target for integrated control of F. proliferatum and its associated mycotoxin risk.