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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
PubMed

Insights

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.
Keywords:
FpLaeAFusarium proliferatumfumonisin B1jasmonic acidpathogenicity

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