Identification and characterization of Cap1, the adenylate cyclase-associated protein (CAP) ortholog in Ustilago maydis

Ustilago maydis, the causal agent of corn smut, has emerged as a basidiomycete model system for signal transduction, dimorphism, and disease development. The well-characterized cAMP/PKA signaling pathway mediates filamentation in response to environmental cues, and in the absence of the cAMP signal, haploid cells grow filamentously. Prior to this report, the G-protein alpha and beta subunits, Gpa3 and Bpp1, respectively, were demonstrated to function upstream of adenylate cyclase, Uac1. In other fungal systems, adenylate cyclase is also positively regulated by the adenylate cyclase-associated protein (CAP). A CAP ortholog, Cap1, was identified by sequence homology in the U. maydis genome. Yeast 2-hybrid analysis indicated that Cap1 bound itself and the C-terminus of Uac1. Deletion of cap1 resulted in abnormal colony formation with filamentous cells that reverted to budding in the presence of exogenous cAMP. The Δcap1 strains had a reduced ability to form mating filaments compared to wild type strains. Pathogenicity was significantly reduced in Δcap1 strains in wild type and solopathogenic genetic backgrounds. These results suggest that Cap1 is an additional component of the cAMP/PKA signaling pathway that coordinates production of cAMP upstream of Uac1.

Research highlights
► Deletion of cap1 in Ustilago maydis generates a filamentous phenotype that is corrected by exogenous cAMP.