Protein kinase A encoded by TPK2 regulates dimorphism of Candida albicans

External signals induce the switch from a yeast to a hyphal growth form in the fungal pathogen Candida albicans, We demonstrate here that the catalyti c subunit of a protein kinase A (PKA) isoform encoded by TPK2 is required f or internal signalling leading to hyphal differentiation, TPK2 complements the growth defect of a Saccharomyces cerevisiae tpk1-3 mutant and Tpk2p is able to phosphorylate an established PKA-acceptor peptide (kemptide), Delet ion of TPK2 blocks morphogenesis and partially reduces virulence, whereas T PK2 overexpression induces hyphal formation and stimulates agar invasion, T he defective tpk2 phenotype is suppressed by overproduction of known signal ling components, including Efg1p and Cek1p, whereas TPK2 overexpression rec onstitutes the cek1 but not the efg1 phenotype. The results indicate that P KA activity of Tpk2p is an important contributing factor in regulating dimo rphism of C. albicans.