Abstract
The current research on cellular heat stress management focuses on the roles of heat shock proteins (HSPs) and the proteostasis network under severe stress conditions. The mild, fever-type stress and the maintenance of membrane homeostasis are less well understood. Herein, we characterized the acute effect of mild, fever-range heat shock on membrane organization, and HSP synthesis and localization in two mammalian cell lines, to delineate the role of membranes in the sensing and adaptation to heat. A multidisciplinary approach combining ultrasensitive fluorescence microscopy and lipidomics revealed the molecular details of novel cellular “eustress”, when cells adapt to mild heat by maintaining membrane homeostasis, activating lipid remodeling, and redistributing chaperone proteins. Notably, this leads to acquired thermotolerance in the complete absence of the induction of HSPs. At higher temperatures, additional defense mechanisms are activated, including elevated expression of molecular chaperones, contributing to an extended stress memory and acquired thermotolerance.
Highlights
Based on the intensity of stress, the heat stress (HS) is currently classified as mild or severe
To be able to compare the results with image-based fluorescence correlation spectroscopy (ImFCS) studies (Fig. 5), we employed a chinese hamster ovary (CHO) cell line expressing glycosylphosphatidyl-inositol-anchored monomeric green fluorescent protein (GPI-mGFP)[20]
Out of the five major heat shock proteins (HSPs) examined, only HSP25, HSP70, and GRP78 were induced by moderate (42.5 °C) and severe (44 °C) heat; no HSP induction was observed when the cells were treated with mild heat (40 °C) for 20 min (Fig. 1)
Summary
Based on the intensity of stress, the heat stress (HS) is currently classified as mild or severe. Considerable evidence has accumulated in favor of the “membrane sensor (thermometer) hypothesis”, which predicts that plasma membrane alterations affect the extent of HSP activation[7,8]. This is especially pertinent to mild HS, a condition present during fever in vertebrates[8,9,10]. The key consequences of the membrane lipid-controlled sensing and signaling of HS include membrane lipid rearrangement, generation of signaling lipids via activation of various lipases, and de novo synthesis of mediator-type lipids These have been recently reviewed in various yeast, plant, and mammalian species[11,12,13,14,15,16]
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