真核生物转录起始因子eIF5A是一类在真核生物中高度保守的基因家族，调控真核生物生长发育的多个生物学过程。
中科院遗传与发育生物研究所左建儒研究组最近的研究发现，拟南芥eIF5A-2/FBR12通过细胞分裂素信号通路调控拟南芥根木质部的发育。eIF5A-2/FBR1通过与细胞分裂素受体基因（AHK）以及下游磷酸传递蛋白基因（AHP）的遗传互作，调控原生木质部的分化与发育。eIF5A-2蛋白与受体AHK4以及AHP1形成一个蛋白复合体，抑制细胞分裂素信号通路负调控因子AHP6的表达，从而调控根原生木质部的分化。该研究发现了细胞分裂素信号转导机制的一种新的机制。
该研究结果10月26日在线发表于The Plant Cell。左建儒研究组的任勃博士和陈庆国博士为论文的共同第一作者。
该研究项目得到了国家自然科学基金和植物基因组学国家重点实验室的资助。（生物谷Bioon.com）
生物谷推荐的英文摘要
The Plant Cell DOI:10.1105/tpc.113.116236
The Arabidopsis Eukaryotic Translation Initiation Factor eIF5A-2 Regulates Root Protoxylem Development by Modulating Cytokinin Signaling[W]
Bo Rena，1， Qingguo Chena，b，1， Sulei Honga，b， Wenming Zhaoa，b， Jian Fenga，b， Haizhong Fenga and Jianru Zuoa，2
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.
