|Author||Ren, Bo ♦ Chen, Qingguo ♦ Hong, Sulei ♦ Zhao, Wenming ♦ Feng, Jian ♦ Feng, Haizhong ♦ Zuo, Jianru|
|Source||World Health Organization (WHO)-Global Index Medicus|
|Publisher||American Society of Plant Biologists|
|File Format||HTM / HTML|
|Subject Domain (in DDC)||Natural sciences & mathematics ♦ Chemistry & allied sciences ♦ Life sciences; biology ♦ Physiology & related subjects ♦ Biochemistry ♦ Genetics and evolution ♦ Natural history of organisms ♦ Technology ♦ Medicine & health ♦ Human anatomy, cytology, histology ♦ Human physiology ♦ Pharmacology and therapeutics|
|Subject Domain (in MeSH)||Plant Structures ♦ Anatomy ♦ Eukaryota ♦ Organisms ♦ Heterocyclic Compounds ♦ Amino Acids, Peptides, and Proteins ♦ Chemical Actions and Uses ♦ Chemicals and Drugs ♦ Chemical Phenomena ♦ Genetic Phenomena ♦ Biological Sciences|
|Subject Keyword||Discipline Botany ♦ Arabidopsis Proteins ♦ Metabolism ♦ Arabidopsis ♦ Genetics ♦ Cytokinins ♦ Peptide Initiation Factors ♦ Plant Roots ♦ Growth & Development ♦ Rna-binding Proteins ♦ Mutation ♦ Plant Growth Regulators ♦ Signal Transduction ♦ Xylem ♦ Journal Article ♦ Research Support, Non-u.s. Gov't|
|Abstract||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.|
|Description||Country affiliation: China
Author Affiliation: Ren B ( State Key Laboratory of Plant Genomics and National Plant Gene Research Center, Institute of Genetics and Developmental Biology, Chinese Academy of Sciences, Beijing 100101, China.)
|Educational Role||Student ♦ Teacher|
|Age Range||above 22 year|
|Educational Use||Reading ♦ Research ♦ Self Learning|
|Education Level||UG and PG|
|Learning Resource Type||Article|
|Publisher Place||United States|
|Journal||THE PLANT CELL ONLINE|
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