A model of regulation of stress signaling by Mi-2β. Mi-2β and JUNB co-occupancy at AP1 sites provide a transcriptionally repressive complex that restricts chromatin and expression of stress response genes including c-JUN. Reduction of Mi-2β by physical or genetic insult causes induction and recruitment of c-JUN at AP1 sites that increase chromatin accessibility and transcription, possibly by displacing Mi-2β and/or by recruiting chromatin modifiers such as histone acetyltransferases (HATs). The transient nature of activation of the c-JUN complex allows for rapid reinstatement of Mi-2β–JUNB repressive activities at AP1 sites and rerepression of stress response genes.