microbiology, Vol 141, 1559-1566, Copyright © 1995 by Society for General Microbiology
Constitutive glucose-induced activation of the Ras-cAMP pathway and aberrant stationary-phase entry on a glucose-containing medium in the Saccharomyces cerevisiae glucose-repression mutant hex2
F Dumortier, JC Arguelles and JM Thevelein
Laboratorium voor Moleculaire Celbiologie, Katholieke Universiteit te Leuven, Flanders, Belgium.
Addition of glucose to cells of the yeast Saccharomyces cerevisiae growing
on a nonfermentable carbon source triggers a rapid, transient increase in
the cAMP level. The occurrence of this cAMP spike appears to be correlated
inversely with the glucose-repression state of the cells. This was also
observed for the hex2 mutant, which is deficient in glucose repression and
which displayed the cAMP signal constitutively. When cells of the hex2
mutant were starved for nitrogen on a glucose-containing medium, they
rapidly lost viability, similarly to mutants with overactivation of the
Ras-adenylate cyclase pathway. Flow cytometry measurements showed that G1
arrest of the hex2 mutant under such conditions was incomplete. Trehalose
accumulation, a typical feature of cells entering the stationary phase G0,
was very short-lived in the hex2 mutant under the same conditions. These
results are in agreement with the presence of continuous glucose-triggered
activation of cAMP synthesis in hex2 cells on a glucose-containing
nitrogen- starvation medium. In the course of these experiments a
spontaneous suppressor mutant, shx (for suppressor of hex2), was isolated
which survived nitrogen starvation on a glucose-containing medium much
better than the hex2 strain. It also showed normal G1 arrest and much
longer accumulation of trehalose. The suppressor mutation also caused
inability to grow on nonfermentable carbon sources and absence of invertase
depression, and it was epistatic to hex2 for these characteristics also.
The isolation of this epistatic depression mutation supports the idea that
the defect in glucose repression of the hex2 mutant is the cause of its
rapid loss of viability during nitrogen starvation on a glucose-containing
medium.(ABSTRACT TRUNCATED AT 250 WORDS)
