The SWI/SNF chromatin-remodeling gene AtCHR12 mediates temporary growth arrest in Arabidopsis thaliana upon perceiving environmental stress

Authors

  • Ludmila Mlynárová,

    Corresponding author
    1. Laboratory of Molecular Biology, Plant Sciences Group, Wageningen University and Research Centre (WUR), 6703 HA Wageningen, The Netherlands,
    2. Institute of Plant Genetics and Biotechnology, 94901 Nitra, Slovak Republic,
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  • Jan-Peter Nap,

    1. Centre for BioSystems Genomics (CBSG), PO Box 98, 6700 AB Wageningen, The Netherlands, and
    2. Institute for Life Science & Technology, Hanze University Groningen, 9701 DA Groningen, The Netherlands
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  • Ton Bisseling

    1. Laboratory of Molecular Biology, Plant Sciences Group, Wageningen University and Research Centre (WUR), 6703 HA Wageningen, The Netherlands,
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*(fax +31 317 482036; e-mail ludmila.mlynarova@wur.nl).

Summary

One of the earliest responses of plants to environmental stress is establishing a temporary growth arrest that allows adaptation to adverse conditions. The response to abiotic stress requires the modulation of gene expression, which may be mediated by the alteration of chromatin structures. This alteration can be accomplished with the help of chromatin-remodeling enzymes, such as the various SWI/SNF classes of ATPases. Here, we investigate the role of the Arabidopsis SNF2/Brahma-type AtCHR12 chromatin-remodeling gene in plant growth and development in reaction to adverse environmental conditions. We show that the AtCHR12 chromatin-remodeling gene plays a vital role in mediating the temporary growth arrest of Arabidopsis that is induced upon perception of stress. Exposing an AtCHR12 overexpressing mutant to stress conditions leads to growth arrest of normally active primary buds, as well as to reduced growth of the primary stem. In contrast, the AtCHR12 knockout mutant shows less growth arrest than the wild-type when exposed to moderate stress. Without stress, mutant plants are indistinguishable from the wild-type, and the growth arrest response seems to depend on the severity of the stress applied. Modulation of AtCHR12 expression correlates with changes in expression of dormancy-associated genes. This is in agreement with the concept of AtCHR12 participation in priming the plants for the growth arrest response. Our data indicate that AtCHR12-associated growth arrest differs from DELLA-mediated growth restraint. This establishes AtCHR12 as a novel gene involved in the response repertoire of plants that permits flexible modulation of growth in adverse and/or otherwise limiting environments.

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