VdATG24 Is Essential for Fungal Growth, Microsclerotia Formation and Virulence in Verticillium dahliae.

Abstract

In phytopathogenic fungi, ATG24 has been identified as the first and evolutionarily conserved receptor. However, its roles in fungal development and pathogenicity vary among species and necessitate further exploration across more diverse fungal genera. In this study, we dissected the molecular functions and underlying mechanisms of the mitophagy receptor ATG24 homolog in the soil-borne hemibiotrophic fungus Verticillium dahliae. VdATG24 contains a PX domain, a BAR domain, and an AIM (Atg8-family Interacting Motif), and is a crucial component for prohibitins (PHB)-mediated mitophagy triggered by both nitrogen deprivation and a mitophagy-specific activator in V. dahliae. Deletion of VdATG24 inhibited the growth rate, shortened the distance between septa, reduced spore production, and impacted microsclerotia formation of V. dahliae, without altering spore morphology or sporulation mode. Assessments of pathogenicity further demonstrated that VdATG24 contributes to fungal virulence through the promotion of host colonization. Mechanistically, we uncovered that ATG24 mediates melanin biosynthesis, facilitates protein secretion during the infection process, and indirectly attenuates host immunity, as evidenced by the identified key components and associated biological processes/pathways via transcriptome analyses and subsequent experimental verification. Our data collectively underscore the pivotal roles and preliminary molecular mechanisms of VdATG24 in modulating hyphal growth, conidiation, microsclerotia formation, and virulence in V. dahliae.