Title: | Constitutive activation of the Saccharomyces cerevisiae mating response pathway by a MAP kinase kinase from Candida albicans |
Author(s): | Clark KL; Feldmann PJ; Dignard D; Larocque R; Brown AJ; Lee MG; Thomas DY; Whiteway M; |
Address: | "Eukaryotic Genetics Group, Biotechnology Research Institute, National Research Council Canada, Montreal, Quebec, Canada" |
ISSN/ISBN: | 0026-8925 (Print) 0026-8925 (Linking) |
Abstract: | "The HST7 gene of Candida albicans encodes a protein with structural similarity to MAP kinase kinases. Expression of this gene in Saccharomyces cerevisiae complements disruption of the Ste7 MAP kinase kinase required for both mating in haploid cells and pseudohyphal growth in diploids. However, Hst7 expression does not complement loss of either the Pbs2 (Hog4) MAP kinase kinase required for response to high osmolarity, or loss of the Mkk1 and Mkk2 MAP kinase kinases required for proper cell wall biosynthesis. Intriguingly, HST7 acts as a hyperactive allele of STE7; expression of Hst7 activates the mating pathway even in the absence of upstream signaling components including the Ste7 regulator Ste11, elevates the basal level of the pheromone-inducible FUS1 gene, and amplifies the pseudohyphal growth response in diploid cells. Thus Hst7 appears to be at least partially independent of upstream activators or regulators, but selective in its activity on downstream target MAP kinases. Creation of Hst7/Ste7 hybrid proteins revealed that the C-terminal two-thirds of Hst7, which contains the protein kinase domain, is sufficient to confer this partial independence of upstream activators" |
Keywords: | "Alleles Amino Acid Sequence Base Sequence Candida albicans/*enzymology/genetics Cell Differentiation Enzyme Activation *Fungal Proteins Gene Deletion Genes, Fungal Genetic Complementation Test Infertility *Mitogen-Activated Protein Kinase Kinases Molecula;" |
Notes: | "MedlineClark, K L Feldmann, P J Dignard, D Larocque, R Brown, A J Lee, M G Thomas, D Y Whiteway, M eng L19195/PHS HHS/ Research Support, Non-U.S. Gov't Research Support, U.S. Gov't, P.H.S. Germany 1995/12/20 Mol Gen Genet. 1995 Dec 20; 249(6):609-21. doi: 10.1007/BF00418030" |