Chaperonin-mediated winter cold response via circadian clock components in Arabidopsis.

Plants adapt to winter through two key strategies: vernalization, which enables flowering after prolonged cold, and cold acclimation, which enhances freezing tolerance. Although both require long-term cold perception, how they are integrated remains unclear. We identify the cytosolic chaperonin TCP1 Ring Complex (TRiC)/Chaperonin Containing TCP1 (CCT) complex as a critical upstream regulator of both processes in Arabidopsis. A missense mutation in CCT8 impairs vernalization and freezing tolerance, with reduced expression of VERNALIZATION INSENSITIVE 3 (VIN3) and C-REPEAT BINDING FACTORs (CBFs), central regulators of these processes. TRiC is required for the accumulation of REVEILLE (RVE) transcription factors, core components of the circadian oscillator. In particular, RVE8 activates VIN3 and CBF expression by binding their promoters. Genetic and biochemical evidence shows that TRiC promotes RVE abundance during cold exposure, thereby contributing to VIN3-associated epigenetic silencing of FLOWERING LOCUS C and CBF-dependent freezing tolerance. VIN3 expression is also circadian-regulated and preferentially induced by cold during the subjective day, revealing circadian gating. These findings uncover a TRiC-RVE-VIN3/CBF regulatory framework linking circadian signaling with seasonal cold adaptation, and show how a core protein-folding machinery modulates transcription factors to coordinate developmental processes and stress responses in winter.