Isolation and characterization of abscisic acid-deficient Arabidopsis mutants at two new loci

Authors

  • Karen M. Léon-Kloosterziel,

    1. Department of Genetics, Wageningen Agricultural University, Dreijenlaan 2, 6703 HA, Wageningen, The Netherlands
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  • Marta Alvarez Gil,

    1. Department of Genetics, Wageningen Agricultural University, Dreijenlaan 2, 6703 HA, Wageningen, The Netherlands
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    • Present address: Instituto Nacional de Ciencias Agricolas, Gaveta postal no.1, San Jose de las Layas, La Habana, C.P. 32700, Cuba.

  • Gerda J. Ruijs,

    1. Department of Genetics, Wageningen Agricultural University, Dreijenlaan 2, 6703 HA, Wageningen, The Netherlands
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  • Steven E. Jacobsen,

    1. Department of Plant Biology, University of Minnesota, St Paul, MN 55108, USA
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    • Present address: Division of Biology 156-29, California Institute of Technology, Pasadena, CA 91125, USA.

  • Neil E. Olszewski,

    1. Department of Plant Biology, University of Minnesota, St Paul, MN 55108, USA
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  • Steven H. Schwartz,

    1. MSU-DOE Plant Research Laboratory, Michigan State University, East Lansing, MI 48824-1312, USA
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  • Jan A.D. Zeevaart,

    1. MSU-DOE Plant Research Laboratory, Michigan State University, East Lansing, MI 48824-1312, USA
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  • Maarten Koornneef

    Corresponding author
    1. Department of Genetics, Wageningen Agricultural University, Dreijenlaan 2, 6703 HA, Wageningen, The Netherlands
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*For correspondence (fax +31 317 483146; e-mail maarten.koornneef@botgen.el.wau.nl).

Abstract

Novel Arabidopsis mutants with lowered levels of endogenous abscisic acid (ABA) were isolated. These were selected in a screen for germination in the presence of the gibberellin biosynthesis inhibitor paclobutrazol. Another mutant was isolated in a screen for NaCl tolerance. The ABA-deficiency was caused by two monogenic, recessive mutations, aba2 and aba3, that were both located on chromosome 1. The mutants showed a phenotype that is known to be characteristic for ABA-deficiency: a reduced seed dormancy and excessive water loss, leading to a wilty phenotype. Double mutant analysis, combining different aba mutations, indicated the leaky nature of the mutations.

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