The capacity for adaptation to changes in intra and extracellular conditions is a universal prerequisite for an organism’s survival and evolution. The existence of molecular mechanisms responsible for repair and adaptation, many of which are greatly conserved across nature, endows the cell with the plasticity it requires to adjust to its ever-changing environment, a homeostatic event that is termed the stress response.

 

Through the sensing and transduction of the stress signal into the different cellular compartments, a genetic reprogramming occurs that leads, on the one hand, to a transient arrest of normal cellular processes, such as a decrease in the expression of house-keeping genes and protein synthesis and, on the other hand, to an enhancement of the expression of genes encoding stress proteins. These include molecular chaperones responsible for maintaining protein folding, transcription factors that further modulate gene expression and a diverse network of players including membrane transporters and proteins involved in repair, degradation and detoxification pathways, nutrient metabolism and osmolyte production, amongst others.

 

Survival and growth resumption necessarily implies successful cellular adaptation to the new conditions as well as the repair of damage incurred to the cell that would otherwise compromise its viability. Although specific stress conditions elicit distinct cellular responses, there is an underlying gene expression program that is commonly activated when the organism is shifted to sub-optimal conditions. Ultimately, the stress response, tailored to the intensity of the insult, represents a graded combination of both specific and general mechanisms available, and this must be employed with precision so as to ensure successful adaptation without compromising cell viability.