Abstract
In Arabidopsis thaliana, the FLOWERING LOCUS C (FLC) gene plays a central role in the repression of the flowering. Transcription of FLC is regulated by epigenetic mechanisms such as covalent histone modifications and histone variant deposition. Here, we reveal the function of histone H2B deubiquitination on the transcriptional activation of FLC. A mutation in the H2B deubiquitinase, SUP32/UBIQUITIN-SPECIFIC PROTEASE 26 (UBP26), resulted in the reduction of FLC expression and an early-flowering phenotype. In the sup32 mutant, H2B monoubiquitination increased at the FLC locus. Furthermore, H3K36 trimethylation decreased and H3K27 trimethylation increased at the FLC locus in the mutant. H3K36 and H3K27 trimethylation is involved in the activation and repression of FLC transcription, respectively. Thus, SUP32 is required for the transcriptional activation of FLC through H2B deubiquitination, which regulates lysine methylation of histone H3.
