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The palmitoyl-CoA ligase Fum16 is part of a Fusarium verticillioides fumonisin subcluster involved in self-protection

Summary

Fusarium verticillioides is a fungus that produces fumonisin B1, a poisonous compound that can contaminate corn and harm human and animal health. Remarkably, the fungus has evolved special protective mechanisms to survive its own poison. This study discovered that five genes in the fungus work together to shield it from fumonisin’s toxic effects by either breaking down the toxin or boosting the production of protective molecules called ceramides in cell membranes.

Background

Fusarium verticillioides produces fumonisin B1 (FB1), a mycotoxin that inhibits ceramide synthase and disrupts sphingolipid biosynthesis, affecting plant, animal, and human health. While the fungus produces this toxin, it must protect itself from self-intoxication through unknown mechanisms. Previous research identified some fumonisin cluster genes involved in self-protection, but the functions of FUM15 and FUM16 remained enigmatic.

Objective

This study aimed to uncover the functions of FUM15 and FUM16 genes in the fumonisin biosynthetic cluster and determine their roles in protecting F. verticillioides from its own mycotoxin FB1. The researchers hypothesized that these genes contribute to self-protection mechanisms through their enzymatic activities.

Results

FUM15 and FUM16 co-localized with ceramide synthase Fum18 to the endoplasmic reticulum. Deletion of FUM15 or FUM16 increased susceptibility to FB1 in F. verticillioides, while expression in yeast provided protection. Fum16 was identified as a functional palmitoyl-CoA ligase through in vitro enzyme assays, while Fum15, a P450 monooxygenase, appeared to detoxify FB1 by reducing extracellular toxin levels.

Conclusion

A five-gene subcluster (FUM15-19) within the fumonisin biosynthetic gene cluster is dedicated to fungal self-protection against FB1. FUM16, FUM17, and FUM18 supplement ceramide biosynthesis as a palmitoyl-CoA ligase and ceramide synthases respectively, while FUM15 likely detoxifies FB1 through chemical modification, and FUM19 represses cluster expression.
  • Published in:mBio,
  • Study Type:Experimental Research,
  • Source: PMID: 39704544
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