The bromodomain protein GTE6 controls leaf development in Arabidopsis by histone acetylation at ASYMMETRIC LEAVES1

  1. Yii Leng Chua1,
  2. Stéphanie Channelière2,
  3. Ellie Mott, and
  4. John C. Gray3
  1. Department of Plant Sciences, University of Cambridge, Cambridge CB2 3EA, United Kingdom

Abstract

The transition from the juvenile to the mature phase during vegetative development in plants is characterized by changes in leaf shape. We show that GENERAL TRANSCRIPTION FACTOR GROUP E6 (GTE6) regulates differences in leaf patterning between juvenile and mature leaves in Arabidopsis. GTE6 encodes a novel small bromodomain-containing protein unique to plants. Mutations in GTE6 disrupt the formation of elliptical leaf laminae in mature leaves, whereas overexpression of GTE6 resulted in elongated juvenile leaves. GTE6 positively regulates the expression of ASYMMETRIC LEAVES1 (AS1), which encodes a myb-domain protein that controls proximodistal patterning of leaves. Using chromatin immunoprecipitation (ChIP) assays, we show that GTE6 is associated with the promoter and the start of the transcribed region of AS1 and up-regulates expression of AS1 through acetylation of histones H3 and H4. Genetic studies demonstrated that AS1 is epistatic to GTE6, indicating that GTE6 regulates AS1 during leaf morphogenesis. Chromatin remodeling at AS1 is a key regulatory mechanism in leaf development, which ensures the continual production of mature leaves following juvenile-adult transition, thereby maintaining the identity of the mature vegetative phase.

Keywords

Footnotes

  • Supplemental material is available at http://www.genesdev.org.

  • Article and publication are at http://www.genesdev.org/cgi/doi/10.1101/gad.352005.

  • 1 Present address: Hutchinson MRC Research Centre, Department of Pathology, University of Cambridge, Hills Road, Cambridge CB2 2XZ, UK

  • 2 Present address: Université Pierre et Marie Curie, 4 Place Jussieu, 75005 Paris, France.

  • 3 Corresponding author. E-MAIL jcg2{at}mole.bio.cam.ac.uk; FAX 44-1223-333953.

    • Accepted July 13, 2005.
    • Received May 16, 2005.
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