Kl. Clark et al., CONSTITUTIVE ACTIVATION OF THE SACCHAROMYCES-CEREVISIAE MATING RESPONSE PATHWAY BY A MAP KINASE KINASE FROM CANDIDA-ALBICANS, MGG. Molecular & general genetics, 249(6), 1995, pp. 609-621
The HST7 gene of Candida albicans encodes a protein with structural si
milarity to MAP kinase kinases. Expression of this gene in Saccharomyc
es cerevisiae complements disruption of the Ste7 MAP kinase kinase req
uired for both mating in haploid cells and pseudohyphal growth in dipl
oids. 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 allel
e 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 activat
ors 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 activa
tors.