The Arabidopsis Eukaryotic Translation Initiation Factor eIF5A-2 Regulates Root Protoxylem Development by Modulating Cytokinin Signaling[W]
The Arabidopsis Eukaryotic Translation Initiation Factor eIF5A-2 Regulates Root Protoxylem Development by Modulating Cytokinin Signaling[W]
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DOI：
10.1105/tpc.113.116236
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发表时间：
2013-10
期刊：
影响因子：
11.6
通讯作者：
Bo Ren;Qingguo Chen;Sulei Hong;Wenming Zhao;Jian Feng;Haizhong Feng;Jianru Zuo
中科院分区：
文献类型：
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作者：
Bo Ren;Qingguo Chen;Sulei Hong;Wenming Zhao;Jian Feng;Haizhong Feng;Jianru Zuo
这项工作表明，拟南芥真核生物翻译起始因子5A-2基因和物理相互作用的细胞分裂素途径的关键信号组分，以特异性地调节根原生木质部的发展。植物激素细胞分裂素调节植物生长和发育的各个方面，包括根维管发育。在拟南芥中，细胞分裂素信号组分的突变导致原生木质部细胞文件的错误指定。生长素通过诱导拟南芥磷酸转移蛋白6（AHP6）的表达拮抗细胞分裂素调节的根原生木质部分化，AHP6是细胞分裂素信号的负调节因子。然而，细胞分裂素调控原生木质部分化的分子机制还不完全清楚。在这里，我们表明，突变拟南芥伏马菌素B1-RESISTANT12（FBR12），它编码真核生物翻译起始因子5A，导致有缺陷的原生木质部发展和细胞分裂素的敏感性降低。FBR 12与细胞分裂素受体细胞分裂素反应1（CRE 1）和下游AHP基因进行遗传相互作用，因为双突变体显示出增强的表型。FBR 12与CRE1和AHP 1形成蛋白复合物，细胞分裂素调节该蛋白复合物的形成。有趣的是，ahp 6部分抑制了fbr 12突变表型，而fbr 12突变导致AHP 6表达增加，这表明FBR 12对AHP 6负调节。与此相一致的是，FBR 12在CRE1表达域的异位表达部分挽救了FBR 12中有缺陷的原生木质部发育，而AHP 6的过表达导致了FBR 12样表型。这些结果定义了高度保守的FBR12在细胞分裂素介导的根原生木质部特化中的调节作用。
This work shows that the Arabidopsis eukaryotic translation initiation factor 5A-2 genetically and physically interacts with key signaling components of the cytokinin pathway to specifically regulate root protoxylem development. The phytohormone cytokinin regulates various aspects of plant growth and development, including root vascular development. In Arabidopsis thaliana, mutations in the cytokinin signaling components cause misspecification of protoxylem cell files. Auxin antagonizes cytokinin-regulated root protoxylem differentiation by inducing expression of ARABIDOPSIS PHOSPHOTRANSFER PROTEIN6 (AHP6), a negative regulator of cytokinin signaling. However, the molecular mechanism of cytokinin-regulated protoxylem differentiation is not fully understood. Here, we show that a mutation in Arabidopsis FUMONISIN B1-RESISTANT12 (FBR12), which encodes a eukaryotic translation initiation factor 5A, causes defective protoxylem development and reduced sensitivity to cytokinin. FBR12 genetically interacts with the cytokinin receptor CYTOKININ RESPONSE1 (CRE1) and downstream AHP genes, as double mutants show enhanced phenotypes. FBR12 forms a protein complex with CRE1 and AHP1, and cytokinin regulates formation of this protein complex. Intriguingly, ahp6 partially suppresses the fbr12 mutant phenotype, and the fbr12 mutation causes increased expression of AHP6, indicating that FBR12 negatively regulates AHP6. Consistent with this, ectopic expression of FBR12 in the CRE1-expressing domain partially rescues defective protoxylem development in fbr12, and overexpression of AHP6 causes an fbr12-like phenotype. These results define a regulatory role of the highly conserved FBR12 in cytokinin-mediated root protoxylem specification.