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The high‐osmolarity glycerol– and cell wall integrity–MAP kinase pathways of Saccharomyces cerevisiae are involved in adaptation to the action of killer toxin HM‐1
Author(s) -
Miyamoto Masahiko,
Furuichi Yasuhiro,
Komiyama Tadazumi
Publication year - 2012
Publication title -
yeast
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.923
H-Index - 102
eISSN - 1097-0061
pISSN - 0749-503X
DOI - 10.1002/yea.2927
Subject(s) - saccharomyces cerevisiae , biology , cell wall , osmotic concentration , yeast , kinase , biochemistry , tonicity , osmotic shock , toxin , turgor pressure , cell , microbiology and biotechnology , biophysics , gene
Fps1p is an aquaglyceroporin important for turgor regulation of Saccharomyces cerevisiae . Previously we reported the involvement of Fps1p in the yeast‐killing action of killer toxin HM‐1. The fps1 cells showed a high HM‐1‐resistant phenotype in hypotonic medium and an HM‐1‐susceptible phenotype in hypertonic medium. This osmotic dependency in HM‐1 susceptibility was similar to those observed in Congo red, but different from those observed in other cell wall‐disturbing agents. These results indicate that HM‐1 exerts fungicidal activity mainly by binding and inserting into the yeast cell wall structure, rather than by inhibiting 1,3‐ β ‐glucan synthase. We next determined HM‐1‐susceptibility and diphospho‐MAP kinase inductions in S. cerevisiae . In the wild‐type cell, expressions of diphospho‐Hog1p and ‐Slt2p, and mRNA transcription of CWP1 and HOR2 , were induced within 1 h after an addition of HM‐1. ssk1 and pbs2 cells, but not sho1 and hkr1 cells, showed HM‐1‐sensitive phenotypes and lacked inductions of phospho‐Hog1p in response to HM‐1. mid2 , rom2 and bck1 cells showed HM‐1‐sensitive phenotypes and decreased inductions of phospho‐Slt2p in response to HM‐1. From these results, we postulated that the Sln1–Ypd1–Ssk1 branch of the high‐osmolality glycerol (HOG) pathway and plasma membrane sensors of the cell wall integrity (CWI) pathway detect cell wall stresses caused by HM‐1. We further suggested that activations of both HOG and CWI pathways have an important role in the adaptive response to HM‐1 toxicity. Copyright © 2012 John Wiley & Sons, Ltd.