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Terminal flower 1 (tfl1) from arabidopsis thalianaTerminal flower 1 (tfl1) from arabidopsis thaliana
Structural highlights
FunctionTFL1_ARATH Controls inflorescence meristem identity and is required for maintenance of a indeterminate inflorescence. Prevents the expression of 'APETALA1' and 'LEAFY'. Also plays a role in the regulation of the time of flowering in the long-day flowering pathway. May form complexes with phosphorylated ligands by interfering with kinases and their effectors (By similarity). Evolutionary Conservation Check, as determined by ConSurfDB. You may read the explanation of the method and the full data available from ConSurf. Publication Abstract from PubMedThe Arabidopsis genes FT and TERMINAL FLOWER1 (TFL1) encode related proteins with similarity to human Raf kinase inhibitor protein. FT, and likely also TFL1, is recruited to the promoters of floral genes through interaction with FD, a bZIP transcription factor. FT, however, induces flowering, while TFL1 represses flowering. Residues responsible for the opposite activities of FT and TFL1 were mapped by examining plants that overexpress chimeric proteins. A region important in vivo localizes to a 14-amino-acid segment that evolves very rapidly in TFL1 orthologs, but is almost invariant in FT orthologs. Crystal structures show that this segment forms an external loop of variable conformation. The only residue unambiguously distinguishing the FT and TFL1 loops makes a hydrogen bond with a residue near the entrance of a potential ligand-binding pocket in TFL1, but not in FT. This pocket is contacted by a C-terminal peptide, which also contributes to the opposite FT and TFL1 activities. In combination, these results identify a molecular surface likely to be recognized by FT- and/or TFL1-specific interactors. A divergent external loop confers antagonistic activity on floral regulators FT and TFL1.,Ahn JH, Miller D, Winter VJ, Banfield MJ, Lee JH, Yoo SY, Henz SR, Brady RL, Weigel D EMBO J. 2006 Feb 8;25(3):605-14. Epub 2006 Jan 19. PMID:16424903[1] From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine. References |
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