Chapter 15 : Stress Responses in

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This chapter summarizes the current understanding of stress responses in . Of all the pathogenic species, the stress responses of have been investigated in the greatest depth. Cellular responses to stresses in include heat shock response, osmotic stress response and oxidative stress response. Stress-signaling pathways include mitogen-activated protein kinase (MAPK) pathway, Hog1 pathway and Mkc1 pathway. The chapter describes one's understanding of the molecular mechanisms that regulate stress responses in and, where information is available, , contrasting these mechanisms mainly with those in and . Redox-sensitive antioxidant proteins, with roles in the detoxification of reactive oxygen species, can also act as sensors and regulators of reactive oxygen species-induced signal transduction pathways. Transcription factors that drive stress responses includes Cap1, Skn7 and Msn4. The structures of Hog1 signaling networks differ between and . As these differences must contribute to the behavior of these pathogens in their hosts, it is important that these differences are addressed at a molecular level. Quantitative mathematical modeling of these responses will provide an invaluable foil to our more classical molecular and genomic approaches.

Citation: Brown A, Haynes K, Gow N, Quinn J. 2012. Stress Responses in , p 225-242. In Calderone R, Clancy C (ed), and Candidiasis, Second Edition. ASM Press, Washington, DC. doi: 10.1128/9781555817176.ch15
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Diagram summarizing the pathways implicated in the adaptation of to stress. See text for details. Most connections between signaling components are indicated by dashed lines, but dotted lines are used to indicate connections between osmotic stress signaling factors in an effort to distinguish them from oxidative stress signaling, particularly with regard to upstream components. doi:10.1128/9781555817176.ch15.f1

Citation: Brown A, Haynes K, Gow N, Quinn J. 2012. Stress Responses in , p 225-242. In Calderone R, Clancy C (ed), and Candidiasis, Second Edition. ASM Press, Washington, DC. doi: 10.1128/9781555817176.ch15
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