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FpLaeA Coordinates Fusarium proliferatum Pathogenesis by Orchestrating Mycotoxin Biosynthesis and Host Immune
Ling Wang1, Shaoqing Tang1, Weiyang Liao1
1State Key Laboratory of Rice Biology and Breeding, China National Rice Research Institute, Hangzhou311401, China.
Journal of Agricultural and Food Chemistry
|August 12, 2026
Summary
The methyltransferase FpLaeA is crucial for Fusarium proliferatum pathogenicity, regulating fumonisin B1 (FB1) production and fungal growth. Targeting FpLaeA offers a strategy for controlling rice diseases and mycotoxin contamination.
Area of Science:
- * Mycology
- * Plant Pathology
- * Molecular Biology
Background:
- * Fusarium proliferatum causes significant crop losses through rice spikelet rot.
- * Contamination of grains with fumonisins poses a serious health risk.
- * Understanding fungal regulatory mechanisms is key to developing control strategies.
Purpose of the Study:
- * To investigate the role of the methyltransferase FpLaeA in Fusarium proliferatum pathogenicity.
- * To elucidate the regulatory functions of FpLaeA in fungal development, toxin production, and host interaction.
- * To identify FpLaeA as a potential target for integrated disease and mycotoxin management.
Main Methods:
- * Gene deletion to create a ΔFplaeA mutant.
- * Analysis of fungal growth, conidiation, and β-1,3-glucan accumulation.
- * Quantification of fumonisin B1 (FB1) and assessment of related gene expression.
- * Measurement of alanine levels and sphingolipid homeostasis.
- * Evaluation of invasive hyphal growth and secretion of pectate lyase (PL) and polygalacturonase (PG).
- * Measurement of jasmonic acid (JA) levels and expression of JA biosynthetic genes in infected plants.
Main Results:
- * Deletion of FplaeA (ΔFplaeA) impaired conidiation and increased β-1,3-glucan.
- * The ΔFplaeA mutant did not produce fumonisin B1 (FB1), with downregulated biosynthetic genes, depleted alanine, and disrupted sphingolipid homeostasis.
- * Invasive hyphal growth and secretion of PL and PG were reduced in ΔFplaeA.
- * ΔFplaeA infection activated plant jasmonic acid (JA)-mediated defenses, indicated by elevated JA levels and upregulated JA biosynthetic genes.
Conclusions:
- * FpLaeA is an essential global regulator of Fusarium proliferatum pathogenicity.
- * FpLaeA controls fumonisin B1 (FB1) biosynthesis, fungal development, and virulence factor secretion.
- * FpLaeA plays a role in fungal immune evasion by modulating plant defense responses.
- * FpLaeA is a promising target for integrated control of F. proliferatum and its associated mycotoxin risks.
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