Disruption of MaPigA , a phosphatidylinositol‐ N ‐acetylglucosaminyltransferase subunit gene, promotes cuticle penetration and immune evasion through enhancing cell wall α‐1,3‐glucan in Metarhizium anisopliae

BACKGROUND Metarhizium anisopliae is a major entomopathogenic fungus used in insect pest control. Its pathogenicity hinges on the ability to breach the insect cuticle and evade host immunity, the latter of which is mediated by a reduced host recognition of fungal cell wall components. This study investigated the role of MaPigA , a gene encoding a subunit of the phosphatidylinositol‐ N ‐acetylglucosaminyltransferase (GPI‐GnT) complex, in the virulence of M. anisopliae. RESULTS Disruption of MaPigA significantly enhanced fungal virulence against locusts. Relative to the wild‐type (WT) strain, the Δ MaPigA strain of M. anisopliae applied topically and by hemocoelic injection showed a reduction in median lethal time (LT₅₀) by 1.03 and 0.71 days, respectively. This enhanced virulence was characterized by accelerated cuticle penetration, evidenced by enhanced germination and appressorium formation on locust hindwings, and increased immune evasion, manifested as a significant suppression of host phenoloxidase activity, defensin gene expression, and hemocoelic nodulation. MaPigA deletion was shown to trigger a 21.2% increase in cell wall α‐1,3‐glucan content, which augmented conidial surface hydrophobicity and biofilm formation. This alteration facilitated host cuticle adhesion and likely contributed to immune evasion. CONCLUSION The targeted disruption of MaPigA enhanced the virulence of M. anisopliae by promoting α‐1,3‐glucan accumulation in the cell wall, thereby improving host infection efficiency without compromising fungal growth kinetics. These findings indicate that MaPigA affects the regulation of α‐1,3‐glucan, perhaps indirectly and adaptively, with consequences for virulence.