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The Arabidopsis det3 mutant reveals a central role for the vacuolar H(+)-ATPase in plant growth and development

Academic Article
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Overview

authors

  • Schumacher, K.
  • Vafeados, D.
  • McCarthy, M.
  • Sze, H.
  • Wilkins, T.
  • Chory, Joanne

publication date

  • December 1999

journal

  • Genes & Development  Journal

abstract

  • In all multicellular organisms growth and morphogenesis must be coordinated, but for higher plants, this is of particular importance because the timing of organogenesis is not fixed but occurs in response to environmental constraints. One particularly dramatic developmental juncture is the response of dicotyledonous seedlings to light. The det3 mutant of Arabidopsis develops morphologically as a light-grown plant even when it is grown in the dark. In addition, it shows organ-specific defects in cell elongation and has a reduced response to brassinosteroids (BRs). We have isolated the DET3 gene by positional cloning and provide functional and biochemical evidence that it encodes subunit C of the vacuolar H(+)-ATPase (V-ATPase). We show that the hypocotyl elongation defect in the det3 mutant is conditional and provide evidence that this is due to an alternative mechanism of V-ATPase assembly. Together with the expression pattern of the DET3 gene revealed by GFP fluorescence, our data provide in vivo evidence for a role for the V-ATPase in the control of cell elongation and in the regulation of meristem activity.

subject areas

  • Amino Acid Sequence
  • Animals
  • Arabidopsis
  • Cloning, Molecular
  • Evolution, Molecular
  • Gene Expression Regulation, Developmental
  • Gene Expression Regulation, Enzymologic
  • Gene Expression Regulation, Plant
  • Humans
  • Light
  • Molecular Sequence Data
  • Phylogeny
  • Proton Pumps
  • Proton-Translocating ATPases
  • Sequence Alignment
  • Sequence Homology, Amino Acid
  • Vacuolar Proton-Translocating ATPases
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Research

keywords

  • Arabidopsis
  • V-ATPase
  • brassinosteroids
  • cell expansion
  • det3
  • positional cloning
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Identity

PubMed Central ID

  • PMC317205

International Standard Serial Number (ISSN)

  • 0890-9369

Digital Object Identifier (DOI)

  • 10.1101/gad.13.24.3259

PubMed ID

  • 10617574
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Additional Document Info

start page

  • 3259

end page

  • 3270

volume

  • 13

issue

  • 24

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