LNK1/2 mediate circadian-gated thermotolerance by regulating ROS homeostasis and activating HSFA8-dependent feedback to maintain temperature compensation

accumulation that enhances heat resistance. HSFA8, whose transcriptional activation is highly dependent on LNK1/2, contributes to circadian stability through a feedback mechanism that fine-tunes temperature compensation. Together, these findings establish LNK1/2 as key regulators of circadian timing, ROS signaling, and HSFA8-dependent feedback that coordinate thermotolerance while preserving circadian homeostasis.