The cAMP signaling pathway in Fusarium verticillioides is important for conidiation, plant infection, and stress responses but not fumonisin production.

Fusarium verticillioides is one of the most important fungal pathogens of maize. Mycotoxin, fumonisins produced by this pathogen pose a threat to human and animal health. Because cAMP signaling has been implicated in regulating diverse developmental and infection processes in fungal pathogens, in this study, we aimed to elucidate the function of the cAMP-protein kinase A (PKA) pathway in toxin production and plant infection in F. verticillioides. Targeted deletion mutants were generated for the CPK1 and FAC1 genes that encode a catalytic subunit of PKA and the adenylate cyclase, respectively. Defects in radial growth and macroconidiation were observed in both the cpk1 and fac1 deletion mutants. The fac1 mutant also was significantly reduced in virulence and microconidiation but increased in tolerance to heat and oxidative stresses. These phenotypes were not observed in the cpk1 mutant, indicating that additional catalytic subunit of PKA must exist and function downstream from FAC1. The fac1 mutant formed microconidia mainly in false heads. The expression levels of the hydrophobin genes HYD1 and HYD2, which are known to be associated with change in formation of microconidia, were significantly reduced in the fac1 mutant. Expression of F. verticillioides GSY2 and HSP26 genes, two other putative downstream targets of FAC1, was increased in the fac1 mutant and may be associated with its enhanced stress tolerance. Although fumonisin production was normal, biosynthesis of bikaverin was increased in the fac1 mutant, suggesting that FAC1 and cAMP signaling may have pathway-or metabolite-specific regulatory roles in secondary metabolism. Overall, the pleiotropic defects of the fac1 deletion mutant indicate that the cAMP-PKA pathway is involved in growth, conidiation, bikaverin production, and plant infection in F. verticillioides.