Xin Xin, Jinlong Li, Shu Wang, Yunjiao Pan, Linhan Ye, Huiru Ma, Jiedao Zhang, Xiang Li, Wei Yang, Shuxin Zhang

Abstract 

The vernalization-mediated suppression of FLOWERING LOCUS C (FLC), a central flowering repressor, requires the coordinated action of non-coding RNA (COOLAIR/COLDAIR) and polycomb repressive complex 2 (PRC2)-mediated epigenetic silencing. However, the mechanistic integration of non-coding RNA transcription and PRC2 function during cold exposure remains poorly understood. In this study, we identify the R2R3-MYB transcription factor CDC5 as a critical regulator of vernalization-responsive flowering. Although the cdc5-2 mutant exhibits early flowering under normal conditions, it demonstrates delayed flowering after vernalization, along with defects in the low-temperature repression of FLC, non-coding RNA transcription, and H3K27me3 deposition. This study found that vernalization affects the binding of CDC5 to the FLC chromatin, thereby influencing the enrichment of RNA polymerase II on the FLC chromatin as well as the transcription of COOLAIR and COLDAIR. Furthermore, CDC5 physically interacts with PRC2 components, functioning as an important cofactor for H3K27me3 establishment at FLC. Our findings establish a regulatory paradigm where CDC5 coordinates non-coding RNA transcription with PRC2-mediated epigenetic silencing, thereby bridging transcriptional and epigenetic control of FLC during winter-induced flowering regulation.

Paper Linkage:https://onlinelibrary.wiley.com/doi/10.1111/tpj.70600