Brassinosteroid Signaling Recruits Histone 3 Lysine-27 Demethylation Activity to FLOWERING LOCUS C Chromatin to Inhibit the Floral Transition in Arabidopsis  

作　　者：Zicong Li Yang Ou Zhicheng Zhang Jianming Li Yuehui He 

机构地区：[1]Shanghai Center for Plant Stress Biology & National Key Laboratory of Plant Molecular Genetics, CAS Center for Excellence in Molecular Plant Sciences, Chinese Academy of Sciences (CAS), Shanghai 201602, China [2]University of Chinese Academy of Sciences, Beijing 100049, China [3]Shanghai Center for Plant Stress Biology, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences, Shanghai 201602, China [4]These authors contributed equally to this article

出　　处：《Molecular Plant》2018年第9期1135-1146,共12页分子植物（英文版）

基　　金：This work was supported in part by funding from the National Natural Science Foundation of China （grant number 31721001）, the National Key Research and Development Program of China （2017YFA0503803）, and the Chinese Academy of Sciences （XDPB0404）.

摘　　要：The steroid hormone brassinosteroid （BR） plays a broad role in plant growth and development. As the retarded growth in BR-insensitive and BR-deficient mutants causes a strong delay in days to flowering, BR signaling has been thought to promote the floral transition inArabidopsis. In this study, using a developmental measure of flowering time, we show that BR signaling inhibits the floral transition and promotes vegetative growth in the Arabidopsis accessions Columbia and Enkheim-2. We found that BR signaling promotes the expression of the potent floral repressor FLOWERING LOCUS C （FLC） and three FLC homologs to inhibit flow- ering. In the presence of BR, the transcription factor BRASSINAZOLE-RESISTANT1 （BZR1）, together with BES1 -INTERACTING MYC-like proteins （BIMs）, specifically binds a BR- responsive element in the first intron of FLC and further recruits a histone 3 lysine 27 （H3K27） demethylase to downregulate levels of the repressive H3K27 trimethylation mark and thus antagonize Polycomb silencing at FLC, leading to its activation. Taken together, our findings demonstrate that BR signaling inhibits the floral transition inArabidopsis by a novel molecular mechanism in which BR signals are transduced into FLC activation and consequent floral repression.The steroid hormone brassinosteroid （BR） plays a broad role in plant growth and development. As the retarded growth in BR-insensitive and BR-deficient mutants causes a strong delay in days to flowering, BR signaling has been thought to promote the floral transition inArabidopsis. In this study, using a developmental measure of flowering time, we show that BR signaling inhibits the floral transition and promotes vegetative growth in the Arabidopsis accessions Columbia and Enkheim-2. We found that BR signaling promotes the expression of the potent floral repressor FLOWERING LOCUS C （FLC） and three FLC homologs to inhibit flow- ering. In the presence of BR, the transcription factor BRASSINAZOLE-RESISTANT1 （BZR1）, together with BES1 -INTERACTING MYC-like proteins （BIMs）, specifically binds a BR- responsive element in the first intron of FLC and further recruits a histone 3 lysine 27 （H3K27） demethylase to downregulate levels of the repressive H3K27 trimethylation mark and thus antagonize Polycomb silencing at FLC, leading to its activation. Taken together, our findings demonstrate that BR signaling inhibits the floral transition inArabidopsis by a novel molecular mechanism in which BR signals are transduced into FLC activation and consequent floral repression.

关 键 词：BRASSINOSTEROID BR signaling flowering time BZR1 Polycomb silencing FLOWERING LOCUS C 

分 类 号：Q243[生物学—细胞生物学] X173[环境科学与工程—环境科学]