Arabidopsis homologs of components of the SWR1 complex regulate flowering and plant development
Arabidopsis homologs of components of the SWR1 complex regulate flowering and plant development
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DOI：
10.1242/dev.001891
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发表时间：
2007-05-15
期刊：
影响因子：
4.6
通讯作者：
Lee, Ilha
中科院分区：
文献类型：
--
作者：
Choi, Kyuha;Park, Chulmin;Lee, Ilha
酵母中的SWR1复合体（SWR1C）催化H2AZ变体取代核小体H2A，从而确保潜在基因的完全激活。我们比较了拟南芥中SWR1C组分同源突变体的表型。拟南芥SWC6 （AtSWC6）、FRIGIDA 3抑制因子（SUF3）和SWR1的同源基因——光周期独立早花1 （PIE1）的突变，分别导致了类似的发育缺陷，包括叶片呈丝状、顶端优势弱、花多瓣和开花位点C （FLC）的表达减少，这是一种强花抑制因子。染色质免疫沉淀实验表明，AtSWC6和SUF3结合在FLC启动子的近端区域，原生质体转染实验表明，AtSWC6与SUF3共定位。蛋白相互作用分析表明，PIE1、SUF3、AtSWC6和AtSWC2之间形成了一个复合物。此外，H2AZ是SWR1C的底物，可以与PIE1和AtSWC2相互作用。最后，通过RNA干扰或人工microRNA敲低H2AZ基因，导致与atswc6或suf3相似的表型。我们的研究结果有力地支持了swr1c样复合体在拟南芥中的存在，该复合体确保了正常的发育，包括通过FLC的完全激活来抑制花。
The SWR1 complex (SWR1C) in yeast catalyzes the replacement of nucleosomal H2A with the H2AZ variant, which ensures full activation of underlying genes. We compared the phenotype of mutants in the homologs of SWR1C components in Arabidopsis thaliana. Mutations in Arabidopsis SWC6 (AtSWC6), SUPPRESSOR OF FRIGIDA 3 (SUF3) and PHOTOPERIOD-INDEPENDENT EARLY FLOWERING 1 (PIE1), homologs of SWC6, ARP6 and SWR1, respectively, caused similar developmental defects, including leaf serration, weak apical dominance, flowers with extra petals and early flowering by reduction in expression of FLOWERING LOCUS C (FLC), a strong floral repressor. Chromatin immunoprecipitation assays showed that AtSWC6 and SUF3 bind to the proximal region of the FLC promoter, and protoplast transfection assays showed that AtSWC6 colocalizes with SUF3. Protein interaction analyses suggested the formation of a complex between PIE1, SUF3, AtSWC6 and AtSWC2. In addition, H2AZ, a substrate of SWR1C, interacts with both PIE1 and AtSWC2. Finally, knockdown of the H2AZ genes by RNA interference or artificial microRNA caused a phenotype similar to that of atswc6 or suf3. Our results strongly support the presence of an SWR1C-like complex in Arabidopsis that ensures proper development, including floral repression through full activation of FLC.