The HOG signal transduction pathway in the halophilic fungus Wallemia ichthyophaga: identification and characterisation of MAP kinases WiHog1A and WiHog1B
The high-osmolarity glycerol (HOG) pathway is one of the several MAP kinase cascades in fungi. It is the main signal transduction system that is responsible for cellular stress responses, and has primarily been studied in the context of osmotic stress. In the present study, we provide the first insi...
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Veröffentlicht in: | Extremophiles : life under extreme conditions 2013-07, Vol.17 (4), p.623-636 |
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Sprache: | eng |
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Zusammenfassung: | The high-osmolarity glycerol (HOG) pathway is one of the several MAP kinase cascades in fungi. It is the main signal transduction system that is responsible for cellular stress responses, and has primarily been studied in the context of osmotic stress. In the present study, we provide the first insights into the HOG pathway of the obligatory halophilic basidiomycetous fungus
Wallemia ichthyophaga
, with the characterisation of its two Hog1-like kinases: WiHog1A and WiHog1B. These share high similarity to Hog1 kinase from
Saccharomyces cerevisiae
(ScHog1) at the level of amino-acid sequence. While WiHog1A could not optimally complement the function of ScHog1, WiHog1B was a fully functional Hog1-like kinase and could improve the halotolerance of the yeast, compared to the wild-type or the ScHog1-expressing
hog1Δ
strain. In
W. ichthyophaga
cells, Hog1 was constitutively phosphorylated under optimal osmotic conditions and dephosphorylated when the cells were challenged with hypo-osmolar or hyperosmolar stress. This pattern of phosphorylation kinetics is opposite to that of yeast. Transcriptional analysis of these two kinases in
W. ichthyophaga
shows that
WiHOG1B
is more responsive to changes in NaCl concentrations than
WiHOG1A
. Our identification and characterisation of these Hog1-like kinases from
W. ichthyophaga
confirm the existence of the HOG signalling pathway and its role in osmosensing in this halophilic fungus. |
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ISSN: | 1431-0651 1433-4909 |
DOI: | 10.1007/s00792-013-0546-4 |