FIG. 6.

A proposed model for coherent transition from posttranslational control to transcriptional control as stressor level increases. A, At basal condition in the absence of exogenous stressor, a small fraction of preexisting stress proteins are posttranslationally modified to cope with background/endogenous stress. B, At very low stressor levels, more preexisting stress proteins are posttranslationally modified and thus activated to maintain homeostasis. C, At slightly higher stressor levels, even more preexisting stress proteins are posttranslationally modified and activated to maintain homeostasis. D, At considerably higher stressor levels, preexisting stress proteins are exhausted in terms of posttranslational modification; the cellular state cannot be maintained at the baseline level, and transcriptional induction of stress genes and genes responsible for cell cycle arrest, apoptosis, and other functional changes starts to occur. At these stressor levels, loss of cellular homeostasis and altered cellular function/fate may lead to adverse outcomes. The dial denotes the cellular state that is perturbed and needs to be maintained.