The G-protein coupled receptor GPRK contributes to fungal development and full virulence in Metarhizium robertsii.

G-protein-coupled receptor K (GPRK), which is a class VI fungal G-protein-coupled receptor (GPCR), plays a critical role in plant immunity against pathogens by mediating the endocytic pathway, influencing metabolism in response to environmental signals, and regulating asexual reproduction and pathogenic development. However, the function of these proteins in entomopathogenic fungi has rarely been investigated. Accordingly, we characterized MrGPRK, a GPCR in the entomopathogenic fungus Metarhizium robertsii containing a C-terminal seven-transmembrane and a conserved regulator of G protein signaling domain, and found that it localized to endosomes. Mutant phenotype assays showed that a ΔMrGprk strain displayed increased defects in radial growth (~28%) and decreased conidial production (~80%) compared with a wild-type strain. Decreased conidiation rates coincided well with the repression of conidiation-related regulatory genes, including three key conidial transcription factors: brlA, abaA, and wetA. MrGprk deficiency impaired full virulence (both topical and injectable inoculations). Further analysis demonstrated that deleting fungal MrGprk decreased the rates of appressorium formation and suppressed the transcription of several genes contributing to appressorial turgor pressure, cuticle penetration, and pH regulation. Additionally, the ΔMrGprk strain showed higher cyclic (cAMP) levels, suggesting that this GPCR is critical for cAMP signal transduction. In summary, MrGPRK was found to contribute to vegetative growth, conidial production, and full virulence of M. robertsii. These findings are conducive to a better understanding of the roles of GPCRs in the development and pathogenicity of entomopathogenic fungi.