# FpFumB Is Required for Basic Biological Processes and Virulence in Fusarium proliferatum by Modulating DNA Repair Through Interaction with FpSae2

## TL;DR

This study shows that FpFumB is essential for growth, DNA repair, and virulence in the fungus Fusarium proliferatum.

## Contribution

The novel finding is that FpFumB modulates DNA repair and pathogenicity by interacting with FpSae2 in Fusarium proliferatum.

## Key findings

- Loss of FpFumB causes defects in growth, sporulation, stress tolerance, and virulence.
- FpFumB interacts with FpSae2, a DNA repair protein, to influence DNA damage response and pathogenicity.
- Malate supplementation can restore growth defects caused by FpFumB loss.

## Abstract

Fumarase plays a pivotal role in the tricarboxylic acid cycle, but its functions in plant pathogenic fungi are not well understood. We identified two fumarase genes in Fusarium proliferatum and generated individual deletion mutants. Loss of FpFumB led to defects in growth, sporulation, stress tolerance, and virulence. Exogenous malate supplementation restored growth defects. Site-directed mutagenesis of residues G452 and A463 reduced FpFumB enzyme activity. Transcriptomic analysis identified significant changes in gene expression related to different metabolic pathways. Protein interaction assays showed that FpFumB interacts with the DNA repair protein FpSae2. Both ΔFpFumB and ΔFpSae2 mutants displayed altered sensitivity to DNA-damaging agents and reduced virulence, indicating that FpFumB modulates DNA repair and pathogenicity through its interaction with FpSae2. Together, these findings highlight FpFumB as a key regulator of basic biological processes, DNA damage repair, and virulence in Fusarium proliferatum.