Proteasome-Mediated Degradation of FRIGIDA Modulates Flowering Time in Arabidopsis during Vernalization

Proteasome-Mediated Degradation of FRIGIDA Modulates Flowering Time in Arabidopsis during Vernalization
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蛋白酶体介导的 FRIGIDA 降解调节拟南芥春化过程中的开花时间

DOI:
10.1105/tpc.114.132738
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发表时间:
2014-12-01
期刊:
影响因子:
11.6
通讯作者:
Yang, Yongping
Yang, Yongping
中科院分区:
生物学1区
文献类型:
--
作者:
Hu, Xiangyang;Kong, Xiangxiang;Yang, Yongping

文献摘要

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拟南芥的冬一年生种质需要暴露于冷胁迫或春化以通过FRIGIDA(FRI)启动开花。FRI作为支架蛋白来招募几种染色质修饰剂,这些修饰剂可表观遗传地修饰开花基因。在这里,我们报告,蛋白酶体介导的FRI降解调节开花春化过程中在拟南芥。我们的遗传和生化实验表明,FRI直接与BTB(Bric-a-Brac/Tramtrack/Broad Complex)蛋白LIGHT-RESPONSE BTB 1(LRB 1)和LRB 2以及CULLIN 3A(CUL 3A)泛素-E3连接酶在体外和体内相互作用,导致FRI在春化过程中的蛋白酶体降解。FRI的降解伴随着长的非编码RNA ColdAIR水平的增加,其降低了FLOWLOCUS C染色质中组蛋白H3 Lys 4三甲基化(H3 K4 me 3)的水平以促进开花。此外,我们发现冷诱导的WRKY 34转录因子与CUL 3A启动子区的W-box结合,从而调节CUL 3A的表达。WRKY 34的缺失抑制了CUL 3A的转录,增强了FRI蛋白的稳定性,导致春化后开花延迟。相反,WRK 34的过表达通过诱导CUL 3A积累促进FRI降解和早开花。总之,这些数据表明,WRKY 34诱导的和CUL 3A依赖的蛋白水解FRI调节开花春化反应。
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.