Cotranscriptional splicing is required in the cold to produce isoforms that repress .

Plants use seasonal cold to time the transition to reproductive development. Short- and long-term cold exposure is registered via parallel transcriptional shutdown and Polycomb-dependent epigenetic silencing of the major flowering repressor locus (). The cold-induced antisense transcripts () determine the dynamics of transcriptional shutdown, but the thermosensory mechanisms are still unresolved. Here, through a forward genetic screen, we identify a mutation that perturbs cold-induced expression and 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 and RNA 3' processing/cotranscriptional regulators and enhances proximal intron splicing to promote specific isoforms. SMU1 also interacts with ELF7, an RNA Polymerase II Associated Factor (Paf1) component and limits transcription. Cold thus changes cotranscriptional splicing/RNA Pol II functionality in an SMU1-dependent mechanism to promote two different isoforms of that lead to reduced transcription. Such cotranscriptional mechanisms are emerging as important regulators underlying plasticity in gene expression.