Role of the CAMP Signaling Pathway in the Dissemination and Development on Pepper Fruit Anthracnose Disease Caused by

The ascomycete fungus causes severe anthracnose disease on the fruit of sweet pepper and chili pepper ( L.) worldwide. Understanding the biology of would improve the management of fruit anthracnose diseases. The cyclic adenosine monophosphate (cAMP) signaling pathway regulates diverse cellular and physiological processes in several foliar fungal pathogens. We investigated the roles of the cAMP signaling pathway in using pharmaceutical and genetic approaches. Exogenous cAMP was found to increase conidiation, appressorium formation, and anthracnose disease development in . , , and , which regulate the intracellular cAMP level, were deleted by homology-dependent gene replacement. Expectedly, the intracellular cAMP level was significantly decreased in and but increased in . All three deletion mutants exhibited serious defects in multiple fungal developments and pathogenicity, suggesting regulation of the intracellular cAMP level is important for . Notably, exogenous cAMP recovered the defect of in appressorium development, but not penetration, which was further recovered by adding CaCl. This result suggests that CsAc1 is associated with both the cAMP and Ca signaling pathways in . produced morphologically abnormal conidia with reduced tolerance to thermal stress. was completely defective in conidiation in , unlike other foliar pathogens. Taken together, these results demonstrate the importance of cAMP signaling in anthracnose disease caused by .