3w06
Crystal structure of Arabidopsis thaliana DWARF14 Like (AtD14L)Crystal structure of Arabidopsis thaliana DWARF14 Like (AtD14L)
Structural highlights
FunctionKAI2_ARATH Involved in seed germination and seedling development. Essential for plant responses to karrikins, a class of butenolide compounds, structurally similar to strigolactones, released from burning vegetation that stimulate seed germination and enhance seedling photomorphogenesis. KAI2 is not required for strigolactone-mediated responses, but MAX2 is necessary for responses to karrikins and strigolactones.[1] [2] [3] [4] Publication Abstract from PubMedStrigolactones (SLs) are plant hormones that inhibit shoot branching. DWARF14 (D14) inhibits rice tillering and is an SL receptor candidate in the branching inhibition pathway, whereas the close homologue DWARF14-LIKE (D14L) participates in the signaling pathway of karrikins (KARs), which are derived from burnt vegetation as smoke stimulants of seed germination. We provide the first evidence for direct binding of the bioactive SL analogue GR24 to D14. Isothermal titration calorimetry measurements show a D14-GR24 binding affinity in the sub-micromolar range. Similarly, bioactive KAR1 directly binds D14L in the micromolar range. The crystal structure of rice D14 shows a compact alpha-/beta-fold hydrolase domain forming a deep ligand-binding pocket capable of accommodating GR24. Insertion of four alpha-helices between beta6 strand and alphaD helix forms the helical cap of the pocket, although the pocket is open to the solvent. The pocket contains the conserved catalytic triad Ser-His-Asp aligned with the oxyanion hole, suggesting hydrolase activity. Although these structural characteristics are conserved in D14L, the D14L pocket is smaller than that of D14. The KAR-insensitive mutation kai2-1 is located at the prominent long beta6-alphaD1 loop, which is characteristic in D14 and D14L, but not in related alpha-/beta-fold hydrolases. Structures of D14 and D14L in the strigolactone and karrikin signaling pathways.,Kagiyama M, Hirano Y, Mori T, Kim SY, Kyozuka J, Seto Y, Yamaguchi S, Hakoshima T Genes Cells. 2013 Jan 10. doi: 10.1111/gtc.12025. PMID:23301669[5] From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine. References
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