Hu Xiangyang, Kong Xiangxiang, Wang Chuntao, Ma Lan, Zhao Jinjie, Wei Jingjing, Zhang Xiaoming, Loake Gary J, Zhang Ticao, Huang Jinling, Yang Yongping
Key Laboratory for Plant Diversity and Biogeography of East Asia, Kunming Institute of Botany, Chinese Academy of Science, Kunming 650201, China The Germplasm Bank of Wild Species, Kunming Institute of Botany, Chinese Academy of Sciences, Kunming 650201, China Laboratory of Alpine Ecology and Biodiversity, Institute of Tibetan Plateau Research, Chinese Academy of Sciences, Beijing 100101, China
Key Laboratory for Plant Diversity and Biogeography of East Asia, Kunming Institute of Botany, Chinese Academy of Science, Kunming 650201, China The Germplasm Bank of Wild Species, Kunming Institute of Botany, Chinese Academy of Sciences, Kunming 650201, China Laboratory of Alpine Ecology and Biodiversity, Institute of Tibetan Plateau Research, Chinese Academy of Sciences, Beijing 100101, China.
Plant Cell. 2014 Dec;26(12):4763-81. doi: 10.1105/tpc.114.132738. Epub 2014 Dec 23.
Winter-annual accessions of Arabidopsis thaliana require either exposure to cold stress or vernalization to initiate flowering via FRIGIDA (FRI). FRI acts as a scaffold protein to recruit several chromatin modifiers that epigenetically modify flowering genes. Here, we report that proteasome-mediated FRI degradation regulates flowering during vernalization in Arabidopsis. Our genetic and biochemical experiments demonstrate that FRI directly interacts with the BTB (Bric-a-Brac/Tramtrack/Broad Complex) proteins LIGHT-RESPONSE BTB1 (LRB1) and LRB2 as well as the CULLIN3A (CUL3A) ubiquitin-E3 ligase in vitro and in vivo, leading to proteasomal degradation of FRI during vernalization. The degradation of FRI is accompanied by an increase in the levels of the long noncoding RNA ColdAIR, which reduces the level of histone H3Lys4 trimethylation (H3K4me3) in FLOWERING LOCUS C chromatin to promote flowering. Furthermore, we found that the cold-induced WRKY34 transcription factor binds to the W-box in the promoter region of CUL3A to modulate CUL3A expression. Deficiency of WRKY34 suppressed CUL3A transcription to enhance FRI protein stability and led to late flowering after vernalization. Conversely, overexpression of WRK34 promoted FRI degradation and early flowering through inducing CUL3A accumulation. Together, these data suggest that WRKY34-induced and CUL3A-dependent proteolysis of FRI modulate flowering in response to vernalization.
拟南芥的冬性一年生种质需要经历冷胁迫或春化作用，才能通过FRIGIDA（FRI）启动开花。FRI作为一种支架蛋白，招募多种染色质修饰因子，对开花基因进行表观遗传修饰。在此，我们报道蛋白酶体介导的FRI降解在拟南芥春化过程中调控开花。我们的遗传学和生化实验表明，FRI在体外和体内直接与BTB（Bric-a-Brac/Tramtrack/Broad Complex）蛋白光响应BTB1（LRB1）和LRB2以及CULLIN3A（CUL3A）泛素E3连接酶相互作用，导致春化过程中FRI被蛋白酶体降解。FRI的降解伴随着长链非编码RNA ColdAIR水平的增加，ColdAIR降低了开花位点C染色质中组蛋白H3赖氨酸4三甲基化（H3K4me3）的水平，从而促进开花。此外，我们发现冷诱导的WRKY34转录因子与CUL3A启动子区域的W-box结合，调节CUL3A的表达。WRKY34缺失会抑制CUL3A转录，增强FRI蛋白稳定性，并导致春化后开花延迟。相反，WRK34过表达通过诱导CUL3A积累促进FRI降解和提前开花。总之，这些数据表明，WRKY34诱导的、CUL3A依赖的FRI蛋白水解作用响应春化过程调节开花。
