MaCsbD Mediates Thermotolerance and UV-B Resistance in Metarhizium acridum by Regulating DNA Repair, Antioxidant Defense, and Protective Metabolites

Although CsbD-like proteins have been studied extensively in bacteria, their functions in eukaryotes remain largely uncharacterized. Our study investigated the CsbD homolog MaCsbD in the entomopathogenic fungus <i>Metarhizium acridum</i> and uncovered its importance for coping with environmental stress. Loss of <i>MaCsbD</i> resulted in delayed conidial germination, reduced conidial yield, and heightened sensitivity to UV-B irradiation and heat shock. The mechanism analysis revealed that the absence of <i>MaCsbD</i> led to a decline in DNA repair capacity, a weakening of the antioxidant defense mechanism, and a reduction in the induction of heat shock proteins. The determination of the accumulation levels of protective metabolites, melanin, and trehalose in the conidia showed that their contents were significantly decreased. Phylogenetic analysis further revealed that CsbD-like domains are conserved across fungi, suggesting an evolutionary role in stress adaptation. Virulence against locusts was unchanged, indicating that <i>MaCsbD</i> primarily supports abiotic stress tolerance rather than pathogenicity. <i>MaCsbD</i> is therefore required for robust fungal stress responses and identifies a potential target for improving the field performance of fungal biocontrol strains.