[Frontiers in Bioscience S2, 1068-1080, June 1, 2010]

Genomics and proteomics of heat acclimation

Michal Horowitz

Laboratory of Environmental Physiology, The Hebrew University, Jerusalem, Israel

TABLE OF CONTENTS

1. Abstract
2. Introduction
2. Introduction
3. Heat acclimation: physiological criteria and acclimation dynamics
4. Acclimatory neuroplasticity -shifts in temperature thresholds
4.1. Evidence from physiological/electrophysiological studies
4.2. Genomic responses
4.2.1. Does heat acclimation enhance hypothalamic progenitor cell proliferation?
4.2.2. Understanding the hypothalamic transcriptome throughout heat acclimation
4.2.3. Does Heat acclimation affect the epigenetic code?
5. Essential and sufficient genes in heat acclimation and delayed thermal injury
5.1. HSPs affect the thermal injury threshold: an acclimatory profile
5.2. Does HIF-1a play a role? A lesson from the heart and the brain
6. Central-peripheral linkage in heat acclimation
6.1. Effector organs and membrane signaling
6.2. Molecular - physiological linkage in the performance of peripheral organs
7. Heat acclimation mediated cross-tolerance
8. Perspectives
9. Acknowledgement 10. References

1. ABSTRACT

Plasticity of the thermoregulatory system is a key factor for the induction of heat acclimation. Temperature-adaptive shifts in gene expression play an essential role in the processes involved. This review attempts to bridge the gap between the classical physiological heat acclimation profile and the molecular/cellular mechanisms underlying the evolution of the acclimated phenotype. Essential acclimatory modifications linked with thermal tolerance are (i) neuronal plasticity (ii) cytoprotection. Leftward and rightward threshold shifts in these respective functional categories expand the dynamic thermoregulatory range of the acclimated phenotype. Neural plasticity depends on changes in hypothalamic warm/cold sensitive neuron ratio and excitability. Over the course of acclimation, there is marked upregulation of transcripts encoding voltage dependent K+ and Ca2+ channels, neurotransmitters and/or their receptors. Temperature threshold for thermal injury is associated with progressive enhancement of inducible cytoprotective networks including the essential acclimatory components HSP70, HSF1 and HIF-1. Via cross-tolerance, achieved through shared on-call cytoprotective networks, acclimation also renders protection against novel stressors. Collectively, heat acclimation is a within life evolutionarily beneficial phenomenon with a memory, imprinted via epigenetic mechanisms.