Mitogen-activated protein kinase phosphatase is required for genotoxic stress relief in Arabidopsis

  1. Roman Ulm1,5,6,
  2. Ekaterina Revenkova1,3,5,
  3. Gian-Pietro di Sansebastiano1,4,
  4. Nicole Bechtold2, and
  5. Jerzy Paszkowski1
  1. 1Friedrich Miescher Institute, CH-4002 Basel, Switzerland, 2 Institute National de la Recherche Agronomique, Station de Génétique et d'Amélioration des Plantes, F-78026 Versailles, France

Abstract

Genotoxic stress activates complex cellular responses allowing for the repair of DNA damage and proper cell recovery. Although plants are exposed constantly to increasing solar UV irradiation, the signaling cascades activated by genotoxic environments are largely unknown. We have identified an Arabidopsis mutant (mkp1) hypersensitive to genotoxic stress treatments (UV-C and methyl methanesulphonate) due to disruption of a gene that encodes anArabidopsis homolog of mitogen-activated protein kinase phosphatase (AtMKP1). Growth of the mkp1 mutant under standard conditions is indistinguishable from wild type, indicating a stress-specific function of AtMKP1. MAP kinase phosphatases (MKPs), the potent inactivators of MAP kinases, are considered important regulators of MAP kinase signaling. Although biochemical data from mammalian cell cultures suggests an involvement of MKPs in cellular stress responses, there is no in vivo genetic support for this view in any multicellular organism. The genetic and biochemical data presented here imply a central role for a MAP kinase cascade in genotoxic stress signaling in plants and indicate AtMKP1 to be a crucial regulator of the MAP kinase activity in vivo, determining the outcome of the cellular reaction and the level of genotoxic resistance.

Keywords

Footnotes

  • Present addresses: 3Institute for Gene Therapy and Molecular Medicine, Mount Sinai School of Medicine, New York, NY 10029-6574, USA; 4Department of Biological Sciences, Wye College, University of London, Wye, Ashford, Kent TN25 5AH, UK.

  • 5 These authors contributed equally to this work.

  • 6 Corresponding author.

  • E-MAIL ulm{at}fmi.ch; FAX 41-61-697-3976.

  • Article and publication are at www.genesdev.org/cgi/doi/10.1101/gad.192601.

    • Received October 30, 2000.
    • Accepted January 17, 2001.
| Table of Contents

Life Science Alliance