Abstract
There is considerable insight into pathways and genes associated with heat-stress conditions. Most genes involved in stress response have been identified using mutant screens or gene knockdowns. Yet, there is limited understanding of the temporal dynamics of global gene expression in stressful environments. Here, we studied global gene expression profiles during 12 hours of heat stress in the nematode C. elegans. Using a high-resolution time series of increasing stress exposures, we found a distinct shift in gene expression patterns between 3–4 hours into the stress response, separating an initially highly dynamic phase from a later relatively stagnant phase. This turning point in expression dynamics coincided with a phenotypic turning point, as shown by a strong decrease in movement, survival and, progeny count in the days following the stress. Both detectable at transcriptional and phenotypic level, this study pin-points a relatively small time frame during heat stress at which enough damage is accumulated, making it impossible to recover the next few days.
Highlights
Heat-stress results from an exposure to potentially harmful temperature conditions beyond the optimum range of an organism
To avoid the detrimental effects of cytotoxic misfolded protein species and protein aggregates, multiple stress response systems have evolved as a first line of defence to maintain proteostasis, of which the highly-conserved heat-shock response (HSR) pathway is prominent [1,2]
The 1st and 2nd principal components (PCs) place this shift in expression dynamics at 3–4 hours of heat exposure
Summary
Heat-stress results from an exposure to potentially harmful temperature conditions beyond the optimum range of an organism. An increase in the intracellular temperature can interfere with protein homeostasis, leading to an accumulation of misfolded proteins and protein aggregates [1]. To avoid the detrimental effects of cytotoxic misfolded protein species and protein aggregates, multiple stress response systems have evolved as a first line of defence to maintain proteostasis, of which the highly-conserved heat-shock response (HSR) pathway is prominent [1,2]. The connection between the processes involved in stress and aging is further substantiated by the fact that several components of the stress response pathways were found to function as regulators of lifespan [6,7,8]. The evolutionary highly conserved transcription factor HSF-1 is a key component in the initiation of the HSR, as well as a regulator of lifespan [9].
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