Sonneborn A, Bockmühl D P, Gerads M, Kurpanek K, Sanglard D, Ernst J F
Institut für Mikrobiologie, Heinrich-Heine-Universität Düsseldorf, Universitätsstr. 1/Geb. 26.12, D-40225 Düsseldorf, Germany.
Mol Microbiol. 2000 Jan;35(2):386-96. doi: 10.1046/j.1365-2958.2000.01705.x.
External signals induce the switch from a yeast to a hyphal growth form in the fungal pathogen Candida albicans. We demonstrate here that the catalytic subunit of a protein kinase A (PKA) isoform encoded by TPK2 is required for 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). Deletion of TPK2 blocks morphogenesis and partially reduces virulence, whereas TPK2 overexpression induces hyphal formation and stimulates agar invasion. The defective tpk2 phenotype is suppressed by overproduction of known signalling components, including Efg1p and Cek1p, whereas TPK2 overexpression reconstitutes the cek1 but not the efg1 phenotype. The results indicate that PKA activity of Tpk2p is an important contributing factor in regulating dimorphism of C. albicans.
外部信号可诱导真菌病原体白色念珠菌从酵母生长形态转变为菌丝生长形态。我们在此证明，由TPK2编码的蛋白激酶A（PKA）亚型的催化亚基是导致菌丝分化的内部信号传导所必需的。TPK2可弥补酿酒酵母tpk1 - 3突变体的生长缺陷，且Tpk2p能够磷酸化已确定的PKA受体肽（肯普肽）。TPK2的缺失会阻断形态发生并部分降低毒力，而TPK2的过表达会诱导菌丝形成并刺激琼脂侵袭。已知信号成分（包括Efg1p和Cek1p）的过量产生可抑制有缺陷的tpk2表型，而TPK2的过表达可恢复cek1表型，但不能恢复efg1表型。结果表明，Tpk2p的PKA活性是调节白色念珠菌二态性的一个重要因素。
