Genome-Wide Identification and Functional Characterization of the Acyl-CoA Dehydrogenase (ACAD) Family in Fusarium sacchari

Summary

Scientists identified and studied 14 genes responsible for breaking down fatty acids and amino acids in a fungus that causes a major disease in sugarcane plants. By deleting individual genes, they found that two genes (FsACAD-2 and FsACAD-11) were particularly important for the fungus to cause disease. Removing these genes dramatically reduced the fungus’s ability to infect and damage sugarcane, suggesting they could be useful targets for developing new ways to control this costly agricultural disease.

Background

Fusarium sacchari is a primary causal agent of Pokkah boeng disease (PBD), an important fungal disease of sugarcane worldwide that reduces yield by 40-60% in susceptible cultivars. Acyl-CoA dehydrogenases (ACADs) are flavoenzymes involved in β-oxidation of fatty acids and amino acid catabolism in mitochondria. The role of ACADs in F. sacchari pathogenesis has not been previously characterized.

Objective

To identify and functionally characterize all ACAD-encoding genes in F. sacchari genome and investigate their roles in fungal growth, development, stress response, nutrient utilization, and virulence during sugarcane infection.

Results

FsACAD genes were distributed across seven chromosomes and classified into seven phylogenetic clades. Expression patterns were differentially regulated during infection and in response to various fatty acids. FsACAD-deletion mutants showed varied impacts on growth, conidiation, and stress tolerance. FsACAD-2 and FsACAD-11 deletions resulted in severe attenuation of virulence, with double knockout showing additional reduction in disease index.

Conclusion

The study identified FsACADs as important contributors to fatty acid metabolism, amino acid utilization, and virulence in F. sacchari. FsACAD-2 and FsACAD-11 represent potential targets for improved control of Pokkah boeng disease in sugarcane production.
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