Stress Adaptation

Alistair J. P. Brown, Leah E. Cowen, Antonio Di Pietro, Janet Quinn

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40 Citations (Scopus)
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Fungal species display an extraordinarily diverse range of lifestyles. Nevertheless, the survival of each species depends on its ability to sense and respond to changes in its natural environment. Environmental changes such as fluctuations in temperature, water balance or pH, or exposure to chemical insults such as reactive oxygen and nitrogen species exert stresses that perturb cellular homeostasis and cause molecular damage to the fungal cell. Consequently, fungi have evolved mechanisms to repair this damage, detoxify chemical insults, and restore cellular homeostasis. Most stresses are fundamental in nature, and consequently, there has been significant evolutionary conservation in the nature of the resultant responses across the fungal kingdom and beyond. For example, heat shock generally induces the synthesis of chaperones that promote protein refolding, antioxidants are generally synthesized in response to an oxidative stress, and osmolyte levels are generally increased following a hyperosmotic shock. In this article we summarize the current understanding of these and other stress responses as well as the signaling pathways that regulate them in the fungi. Model yeasts such as Saccharomyces cerevisiae are compared with filamentous fungi, as well as with pathogens of plants and humans. We also discuss current challenges associated with defining the dynamics of stress responses and with the elaboration of fungal stress adaptation under conditions that reflect natural environments in which fungal cells may be exposed to different types of stresses, either sequentially or simultaneously.
Original languageEnglish
Pages (from-to)1-23
Number of pages23
JournalMicrobiology spectrum
Issue number4
Publication statusPublished - 14 Jul 2017

Bibliographical note

We thank our numerous friends and colleagues for stimulating discussions about stress adaptation. We are also grateful to the following institutions for generously supporting our research. A.J.P.B was funded by the European Research Council (STRIFE, ERC-2009-AdG-249793), the UK Medical Research Council (MR/M026663/1 and MR/N006364/1), the UK Biotechnology and Biological Research Council (BB/K017365/1), and the Wellcome Trust (080088; 097377). L.E.C. is supported by the Canadian Institutes of Health Research Operating Grants (MOP-86452 and MOP-119520), the Natural Sciences and Engineering Research Council (NSERC) of Canada Discovery Grants (06261 and 462167), an NSERC E.W.R. Steacie Memorial Fellowship (477598), a National Institutes of Health R01 Grant (R01AI120958), and a Canada Research Chair in Microbial Genomics and Infectious Disease. Work in the A.D.P. laboratory is funded by grants from the Spanish Ministerio de Innovación y Competitividad (BIO2013-47870-R), the European Commission (Marie Curie ITN FUNGIBRAIN; FP7-PEOPLE-ITN-607963), and the Junta de Andalucia (BIO296). J.Q. is funded by the UK Biotechnology and Biological Research Council (BB/K016939/1) and the Wellcome Trust (097377).


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