Cotranscriptional splicing is required in the cold to produce COOLAIR isoforms that repress Arabidopsis FLC

成果类型:
Article
署名作者:
Long, Xiaogang; Cai, Yajun; Wang, Huamei; Liu, Yue; Huang, Xiaoyi; Xuan, Hua; Li, Wenjuan; Zhang, Xiaoling; Zhang, Hongya; Fang, Xiaofeng; He, Hang; Xu, Guoyong; Dean, Caroline; Yang, Hongchun
署名单位:
Wuhan University; Hubei Hongshan Laboratory; Peking University; Wuhan University; Wuhan University; Tsinghua University
刊物名称:
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA
ISSN/ISSBN:
0027-11805
DOI:
10.1073/pnas.2407628121
发表日期:
2024-11-19
关键词:
flowering-locus-c nuclear frigida condensation antisense transcripts histone methylation protein induction complex chromosome regulator triggers
摘要:
Plants use seasonal cold to time the transition to reproductive development. Shortand long- term cold exposure is registered via parallel transcriptional shutdown and Polycomb- dependent epigenetic silencing of the Arabidopsis thaliana major flowering repressor locus FLOWERING LOCUS C (FLC). The cold- induced antisense transcripts (COOLAIR) determine the dynamics of FLC transcriptional shutdown, but the thermosensory mechanisms are still unresolved. Here, through a forward genetic screen, we identify a mutation that perturbs cold- induced COOLAIR expression and FLC repression. The mutation is a hypomorphic allele of SUPPRESSORS OF MEC- 8 AND UNC- 52 1 (SMU1), a conserved subunit of the spliceosomal B complex. SMU1 interacts in vivo with the proximal region of nascent COOLAIR and RNA 3 ' processing/ cotranscriptional regulators and enhances COOLAIR proximal intron splicing to promote specific COOLAIR isoforms. SMU1 also interacts with ELF7, an RNA Polymerase II Associated Factor (Paf1) component and limits COOLAIR transcription. Cold thus changes cotranscriptional splicing/RNA Pol II functionality in an SMU1- dependent mechanism to promote two different isoforms of COOLAIR that lead to reduced FLC transcription. Such cotranscriptional mechanisms are emerging as important regulators underlying plasticity in gene expression.