Kim Dong-Hwan, Xi Yanpeng, Sung Sibum
Department of Molecular Biosciences and Institute for Cellular and Molecular Biology, the University of Texas at Austin, TX, United States of America.
PLoS Genet. 2017 Jul 31;13(7):e1006939. doi: 10.1371/journal.pgen.1006939. eCollection 2017 Jul.
The long noncoding RNA COLDAIR is necessary for the repression of a floral repressor FLOWERING LOCUS C (FLC) during vernalization in Arabidopsis thaliana. The repression of FLC is mediated by increased enrichment of Polycomb Repressive Complex 2 (PRC2) and subsequent trimethylation of Histone H3 Lysine 27 (H3K27me3) at FLC chromatin. In this study we found that the association of COLDAIR with chromatin occurs only at the FLC locus and that the central region of the COLDAIR transcript is critical for this interaction. A modular motif in COLDAIR is responsible for the association with PRC2 in vitro, and the mutations within the motif that reduced the association of COLDAIR with PRC2 resulted in vernalization insensitivity. The vernalization insensitivity caused by mutant COLDAIR was rescued by the ectopic expression of the wild-type COLDAIR. Our study reveals the molecular framework in which COLDAIR lncRNA mediates the PRC2-mediated repression of FLC during vernalization.
长链非编码RNA COLDAIR在拟南芥春化过程中对 floral repressor FLOWERING LOCUS C(FLC)的抑制是必需的。FLC的抑制是由多梳抑制复合物2(PRC2)富集增加以及随后FLC染色质上组蛋白H3赖氨酸27(H3K27me3)的三甲基化介导的。在本研究中,我们发现COLDAIR与染色质的结合仅发生在FLC基因座,并且COLDAIR转录本的中心区域对于这种相互作用至关重要。COLDAIR中的一个模块化基序负责在体外与PRC2结合,该基序内的突变减少了COLDAIR与PRC2的结合,导致对春化不敏感。由突变型COLDAIR引起的春化不敏感通过野生型COLDAIR的异位表达得以挽救。我们的研究揭示了COLDAIR lncRNA在春化过程中介导PRC2介导的FLC抑制的分子框架。