Redundant Requirement for a Pair of PROTEIN ARGININE METHYLTRANSFERASE4 Homologs for the Proper Regulation of Arabidopsis Flowering Time1[C][OA]
Redundant Requirement for a Pair of PROTEIN ARGININE METHYLTRANSFERASE4 Homologs for the Proper Regulation of Arabidopsis Flowering Time1[C][OA]
复制标题
DOI：
10.1104/pp.108.124727
复制
发表时间：
2008-07
期刊：
影响因子：
7.4
通讯作者：
Lifang Niu;Yong Zhang;Y. Pei;Chunyan Liu;Xiaofeng Cao
中科院分区：
文献类型：
--
作者：
Lifang Niu;Yong Zhang;Y. Pei;Chunyan Liu;Xiaofeng Cao
CARM1/PRMT4 （COACTIVATOR-ASSOCIATED ARGININE METHYLTRANSFERASE1/PROTEIN ARGININE METHYLTRANSFERASE4）催化精氨酸（Arg）的不对称二甲基化，其在基因调控中的功能仅在动物系统中被了解。在这里，我们将AtPRMT4a和AtPRMT4b描述为哺乳动物CARM1/PRMT4的一对拟南芥同源基因。重组AtPRMT4a和AtPRMT4b能在体外不对称地将组蛋白H3在Arg-2、Arg-17、Arg-26和髓鞘碱性蛋白上二甲基化。AtPRMT4a和AtPRMT4b均表现出核和细胞质分布，并在整个发育过程中在所有组织中普遍表达。谷胱甘肽s转移酶下拉实验显示，AtPRMT4a和AtPRMT4b在体外可形成同型二聚体和异源二聚体，并通过双分子荧光互补进一步证实了异源二聚体的形成。AtPRMT4a和AtPRMT4b基因同时受损导致开花延迟，而AtPRMT4a或AtPRMT4b基因的单突变不会导致重大发育缺陷，这表明AtPRMT4a和AtPRMT4b基因存在冗余。遗传分析还表明，atprmt4a和atprmt4b双突变体表型复制了自主通路突变体。最后，我们发现在atprmt4a和atprmt4b双突变体中，组蛋白H3的Arg-17位点的不对称甲基化大大减少。综上所述，我们的研究结果表明，AtPRMT4a和AtPRMT4b主要通过开花位点c依赖途径对开花时间进行适当调节。
CARM1/PRMT4 (for COACTIVATOR-ASSOCIATED ARGININE METHYLTRANSFERASE1/PROTEIN ARGININE METHYLTRANSFERASE4) catalyzes asymmetric dimethylation on arginine (Arg), and its functions in gene regulation is understood only in animal systems. Here, we describe AtPRMT4a and AtPRMT4b as a pair of Arabidopsis (Arabidopsis thaliana) homologs of mammalian CARM1/PRMT4. Recombinant AtPRMT4a and AtPRMT4b could asymmetrically dimethylate histone H3 at Arg-2, Arg-17, Arg-26, and myelin basic protein in vitro. Both AtPRMT4a and AtPRMT4b exhibited nuclear as well as cytoplasmic distribution and were expressed ubiquitously in all tissues throughout development. Glutathione S-transferase pull-down assays revealed that AtPRMT4a and AtPRMT4b could form homodimers and heterodimers in vitro, and formation of the heterodimer was further confirmed by bimolecular fluorescence complementation. Simultaneous lesions in AtPRMT4a and AtPRMT4b genes led to delayed flowering, whereas single mutations in either AtPRMT4a or AtPRMT4b did not cause major developmental defects, indicating the redundancy of AtPRMT4a and AtPRMT4b. Genetic analysis also indicated that atprmt4a atprmt4b double mutants phenocopied autonomous pathway mutants. Finally, we found that asymmetric methylation at Arg-17 of histone H3 was greatly reduced in atprmt4a atprmt4b double mutants. Taken together, our results demonstrate that AtPRMT4a and AtPRMT4b are required for proper regulation of flowering time mainly through the FLOWERING LOCUS C-dependent pathway.