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

Citation
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
Citations number
40
Categorie Soggetti
Microbiology
Journal title
JOURNAL OF BACTERIOLOGY
ISSN journal
00219193 → ACNP
Volume
182
Issue
9
Year of publication
2000
Pages
2428 - 2437
Database
ISI
SICI code
0021-9193(200005)182:9<2428:CAADOC>2.0.ZU;2-L
Abstract
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.