真核生物轉(zhuǎn)錄起始因子eIF5A是一類(lèi)在真核生物中高度保守的基因家族,，調(diào)控真核生物生長(zhǎng)發(fā)育的多個(gè)生物學(xué)過(guò)程。
中科院遺傳與發(fā)育生物研究所左建儒研究組最近的研究發(fā)現(xiàn),，擬南芥eIF5A-2/FBR12通過(guò)細(xì)胞分裂素信號(hào)通路調(diào)控?cái)M南芥根木質(zhì)部的發(fā)育,。eIF5A-2/FBR1通過(guò)與細(xì)胞分裂素受體基因（AHK）以及下游磷酸傳遞蛋白基因（AHP）的遺傳互作，調(diào)控原生木質(zhì)部的分化與發(fā)育,。eIF5A-2蛋白與受體AHK4以及AHP1形成一個(gè)蛋白復(fù)合體,，抑制細(xì)胞分裂素信號(hào)通路負(fù)調(diào)控因子AHP6的表達(dá)，從而調(diào)控根原生木質(zhì)部的分化,。該研究發(fā)現(xiàn)了細(xì)胞分裂素信號(hào)轉(zhuǎn)導(dǎo)機(jī)制的一種新的機(jī)制,。
該研究結(jié)果10月26日在線(xiàn)發(fā)表于The Plant Cell。左建儒研究組的任勃博士和陳慶國(guó)博士為論文的共同第一作者,。
該研究項(xiàng)目得到了國(guó)家自然科學(xué)基金和植物基因組學(xué)國(guó)家重點(diǎn)實(shí)驗(yàn)室的資助,。（生物谷Bioon.com）
生物谷推薦的英文摘要
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.
