Plants have evolved sophisticated strategies to cope with various environmental stresses. Recent studies have provided insights into the mechanisms of rapid cold stress response through key components including OST1, ICE1, HOS1, and CBFs. However, the mechanisms by which plants modulate the intensity of their cold tolerance in response to fluctuating temperatures remain largely unexplored. In this study, we employed a multidisciplinary approach integrating molecular biology, plant physiology, and genetic methodologies to comprehensively decipher the molecular mechanisms by which HAT1 regulates cold stress responses in plants and further unraveled its cold-dependent posttranslational modification network. We found that under normal conditions, HAT1 acts as a repressor of cold-induced expression of CBF and COR genes, attenuating the cold response. When plants are exposed to cold stress, cold triggers OST1 to phosphorylate HAT1 and facilitates its interaction with HOS1, which subsequently induces ubiquitination and degradation of HAT1. This process alleviates repression of the CBF and COR genes by HAT1 and activates the cold stress response. Thus, our results reveal that HAT1 acts as a brake to prevent excessive cold stress response. The OST1-HOS1 module regulates HAT1 protein stability, allowing plants to dynamically balance growth and cold tolerance in response to environmental signals.