A complex interplay of three R2R3 MYB transcription factors determines the profile of aliphatic glucosinolates in arabidopsis

Ida Elken Sønderby, Meike Burow, Heather C. Rowe, Daniel James Kliebenstein, Barbara Ann Halkier

    156 Citationer (Scopus)

    Abstract

    While R2R3 MYB transcription factors are a large gene family of transcription factors within plants, comprehensive functional data in planta are still scarce. A model for studying R2R3 MYB control of metabolic networks is the glucosinolates (GLSs), secondary metabolites that control plant resistance against insects and pathogens and carry cancer-preventive properties. Three related members of the R2R3 MYB transcription factor family within Arabidopsis (Arabidopsis thaliana), MYB28, MYB29, and MYB76, are the commonly defined regulators of aliphatic GLS biosynthesis. We utilized new genotypes and systems analysis techniques to test the existing regulatory model in which MYB28 is the dominant regulator, MYB29 plays a minor rheostat role, and MYB76 is largely uninvolved. We unequivocally show that MYB76 is not dependent on MYB28 and MYB29 for induction of aliphatic GLSs and that MYB76 plays a role in determining the spatial distribution of aliphatic GLSs within the leaf, pointing at a potential role of MYB76 in transport regulation. Transcriptional profiling of knockout mutants revealed that GLS metabolite levels are uncoupled from the level of transcript accumulation for aliphatic GLS biosynthetic genes. This uncoupling of chemotypes from biosynthetic transcripts suggests revising our view of the regulation of GLS metabolism from a simple linear transcription factor-promoter model to a more modular system in which transcription factors cause similar chemotypes via nonoverlapping regulatory patterns. Similar regulatory networks might exist in other secondary pathways.

    OriginalsprogEngelsk
    TidsskriftPlant Physiology
    Vol/bind153
    Udgave nummer1
    Sider (fra-til)348-363
    Antal sider16
    ISSN0032-0889
    DOI
    StatusUdgivet - maj 2010

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