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Published on: June 23, 2022
FpFumB Is Required for Basic Biological Processes and Virulence in Fusarium proliferatum by Modulating DNA Repair
Yizhou Gao1, Haibo Li1, Yong Liu1
1School of Biological and Chemical Engineering, Zhejiang University of Science and Technology, Hangzhou 310023, China.
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.
Insights
The fumarase enzyme FpFumB is crucial for Fusarium proliferatum growth, sporulation, and virulence. It also interacts with DNA repair protein FpSae2, impacting DNA damage response and pathogenicity.
Area of Science:
- Biochemistry
- Mycology
- Plant Pathology
Background:
- Fumarase is essential for the tricarboxylic acid cycle.
- The role of fumarase in plant pathogenic fungi like Fusarium proliferatum is not well-understood.
Purpose of the Study:
- To investigate the function of fumarase genes in Fusarium proliferatum.
- To elucidate the role of FpFumB in fungal growth, stress tolerance, DNA repair, and virulence.
Main Methods:
- Gene deletion and site-directed mutagenesis of fumarase genes.
- Transcriptomic analysis to identify affected metabolic pathways.
- Protein interaction assays to identify FpFumB interacting partners.
Main Results:
- Deletion of FpFumB impaired fungal growth, sporulation, stress tolerance, and virulence.
- FpFumB interacts with the DNA repair protein FpSae2.
- Mutants lacking FpFumB or FpSae2 showed altered DNA damage sensitivity and reduced virulence.
Conclusions:
- FpFumB is a key regulator of essential biological processes, DNA repair, and pathogenicity in Fusarium proliferatum.
- FpFumB modulates virulence and DNA repair through its interaction with FpSae2.
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