TOPLESS Mediates Auxin-Dependent Transcriptional Repression During <i>Arabidopsis</i> Embryogenesis

  • Heidi Szemenyei
    Plant Biology Laboratory, The Salk Institute for Biological Studies, 10010 North Torrey Pines Road, La Jolla, CA 92037, USA.
  • Mike Hannon
    Plant Biology Laboratory, The Salk Institute for Biological Studies, 10010 North Torrey Pines Road, La Jolla, CA 92037, USA.
  • Jeff A. Long
    Plant Biology Laboratory, The Salk Institute for Biological Studies, 10010 North Torrey Pines Road, La Jolla, CA 92037, USA.

書誌事項

公開日
2008-03-07
DOI
  • 10.1126/science.1151461
公開者
American Association for the Advancement of Science (AAAS)

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説明

<jats:p> The transcriptional response to auxin is critical for root and vascular development during <jats:italic>Arabidopsis</jats:italic> embryogenesis. Auxin induces the degradation of AUXIN/INDOLE-3-ACETIC ACID (AUX/IAA) transcriptional repressors, freeing their binding partners, the AUXIN RESPONSE FACTOR (ARF) proteins, which can activate transcription of auxin response genes. We show that TOPLESS (TPL) can physically interact with IAA12/BODENLOS (IAA12/BDL) through an ETHYLENE RESPONSE FACTOR (ERF)–associated amphiphilic repression (EAR) motif. TPL can repress transcription in vivo and is required for IAA12/BDL repressive activity. In addition, <jats:italic>tpl-1</jats:italic> can suppress the patterning defects of the <jats:italic>bdl-1</jats:italic> mutant. Direct interaction between TPL and ARF5/MONOPTEROS, which is regulated by IAA12/BDL, results in a loss-of-function <jats:italic>arf5</jats:italic> / <jats:italic>mp</jats:italic> phenotype. These observations show that TPL is a transcriptional co-repressor and further our understanding of how auxin regulates transcription during plant development. </jats:p>

収録刊行物

  • Science

    Science 319 (5868), 1384-1386, 2008-03-07

    American Association for the Advancement of Science (AAAS)

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