MaMsb2, a signaling mucin, is involved in conidiation, stress tolerances, and virulence in the entomopathogenic fungus Metarhizium acridum.

Abstract

Entomopathogenic fungi are pivotal microbial resources for crop protection in agriculture, offering a natural and environmentally friendly alternative to chemical pesticides. The signalling mucin gene Msb2 contributes to the modulation of fungal development and virulence, yet its functions have remained unexplored in entomopathogenic fungi. In this study, we aimed to characterize the functions of Msb2 in the model entomopathogenic fungus Metarhizium acridum using gene knockout and complementation strategies. The absence of MaMsb2 led to a delay in conidial germination and an increase in conidial yield due to a shift in the conidiation pattern. Additionally, the MaMsb2-disruption bring about the significantly reduced tolerances to various adversities in M. acridum. Moreover, inactivation of MaMsb2 resulted in the decreased virulence of M. acridum owing to the decrease in conidial hydrophobicity and adhesion, the impairment of appressorium formation, and the reduction of M. acridum growth in the locust haemolymph. To elucidate the molecular mechanisms by which MaMsb2 exerts its influence, we conducted an RNA-seq analysis during appressorium formation. As a result, 880 differentially expressed genes (DEGs) regulated by MaMsb2 were identified. Our data indicated that MaMsb2 governs the appressorium formation of M. acridum by mediating the expression of genes associated with conidia adhesion, appressorium formation, and host cuticle penetration. These findings not only shed light on the multifaceted role of MaMsb2 in the biology of entomopathogenic fungi but also lay the groundwork for future research aimed at unravelling the intricate mechanisms by which MaMsb2 regulates conidiation and pathogenesis.