Calcofluor antifungal action depends on chitin and a functional high-osmolarity glycerol response (HOG) pathway: Evidence for a physiological role ofthe Saccharomyces cerevisiae HOG pathway under noninducing conditions
Lj. Garcia-rodriguez et al., Calcofluor antifungal action depends on chitin and a functional high-osmolarity glycerol response (HOG) pathway: Evidence for a physiological role ofthe Saccharomyces cerevisiae HOG pathway under noninducing conditions, J BACT, 182(9), 2000, pp. 2428-2437
We have isolated several Saccharomyces cerevisiae mutants resistant to calc
ofluor that contain mutations in the PBS2 or HOG1 genes, which encode the m
itogen-activated protein kinase (MAPK) and MAP kinases, respectively, of th
e high-osmolarity glycerol response (HOG) pathway. We report that blockage
of either of the two activation branches of the pathway, namely, SHO1 and S
LN1, leads to partial resistance to calcofluor, while simultaneous disrupti
on significantly increases resistance. However, chitin biosynthesis is inde
pendent of the HOG pathway, Calcofluor treatment also induces an increase i
n salt tolerance and glycerol accumulation, although no activation of the H
OG pathway is detected. Our results indicate that the antifungal effect of
calcofluor depends on its binding to cell wall chitin but also on the prese
nce of a functional HOG pathway. Characterization of one of the mutants iso
lated, pbs2-14, revealed that resistance to calcofluor and HOG-dependent os
moadaptation are two different physiological processes. Sensitivity to calc
ofluor depends on the constitutive functionality of the HOG pathway; when t
his is altered, the cells become calcofluor resistant but also show very lo
w levels of basal salt tolerance. Characterization of some multicopy suppre
ssors of the calcofluor resistance phenotype indicated that constitutive HO
G functionality participates in the maintenance of cell wall architecture,
a conclusion supported by the antagonism observed between the protein kinas
e and HOG signal transduction pathways.