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    Carlactone-independent seedling morphogenesis in Arabidopsis

    Access Status
    Open access via publisher
    Authors
    Scaffidi, A.
    Waters, M.
    Ghisalberti, E.
    Dixon, Kingsley
    Flematti, G.
    Smith, S.
    Date
    2013
    Type
    Journal Article
    
    Metadata
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    Citation
    Scaffidi, A. and Waters, M. and Ghisalberti, E. and Dixon, K. and Flematti, G. and Smith, S. 2013. Carlactone-independent seedling morphogenesis in Arabidopsis. Plant Journal. 76 (1): pp. 1-9.
    Source Title
    Plant Journal
    DOI
    10.1111/tpj.12265
    ISSN
    0960-7412
    School
    Department of Environment and Agriculture
    URI
    http://hdl.handle.net/20.500.11937/46864
    Collection
    • Curtin Research Publications
    Abstract

    Strigolactone hormones are derived from carotenoids via carlactone, and act through the α/β–hydrolase D14 and the F–box protein D3/MAX2 to repress plant shoot branching. While MAX2 is also necessary for normal seedling development, D14 and the known strigolactone biosynthesis genes are not, raising the question of whether endogenous, canonical strigolactones derived from carlactone have a role in seedling morphogenesis. Here, we report the chemical synthesis of the strigolactone precursor carlactone, and show that it represses Arabidopsis shoot branching and influences leaf morphogenesis via a mechanism that is dependent on the cytochrome P450 MAX1. In contrast, both physiologically active Z–carlactone and the non-physiological E isomer exhibit similar weak activity in seedlings, and predominantly signal through D14 rather than its paralogue KAI2, in a MAX2-dependent but MAX1-independent manner. KAI2 is essential for seedling morphogenesis, and hence this early-stage development employs carlactone-independent morphogens for which karrikins from wildfire smoke are specific surrogates. While the commonly employed synthetic strigolactone GR24 acts non-specifically through both D14 and KAI2, carlactone is a specific effector of strigolactone signalling that acts through MAX1 and D14.

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