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DELAY OF GERMINATION 1 mediates a conserved coat-dormancy mechanism for the temperature- and gibberellin-dependent control of seed germination
K. Graeber, A. Linkies, T. Steinbrecher, K. Mummenhoff, D. Tarkowská, V. Turečková, M. Ignatz, K. Sperber, A. Voegele, H. de Jong, T. Urbanová, M. Strnad, G. Leubner-Metzger,
Language English Country United States
Document type Journal Article, Research Support, Non-U.S. Gov't
NLK
Free Medical Journals
from 1915 to 6 months ago
Freely Accessible Science Journals
from 1915 to 6 months ago
PubMed Central
from 1915 to 6 months ago
Europe PubMed Central
from 1915 to 6 months ago
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from 1915-01-01
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from 1915-01-15
- MeSH
- Arabidopsis genetics growth & development physiology MeSH
- Biomechanical Phenomena MeSH
- Diploidy MeSH
- Plants, Genetically Modified MeSH
- Gibberellins metabolism MeSH
- Germination genetics physiology MeSH
- Conserved Sequence MeSH
- Lepidium sativum genetics growth & development physiology MeSH
- Molecular Sequence Data MeSH
- Mutation MeSH
- Arabidopsis Proteins genetics MeSH
- Gene Expression Regulation, Plant MeSH
- Genes, Plant MeSH
- Seeds growth & development MeSH
- Temperature MeSH
- Plant Dormancy genetics physiology MeSH
- Gene Expression Regulation, Developmental MeSH
- Publication type
- Journal Article MeSH
- Research Support, Non-U.S. Gov't MeSH
Seed germination is an important life-cycle transition because it determines subsequent plant survival and reproductive success. To detect optimal spatiotemporal conditions for germination, seeds act as sophisticated environmental sensors integrating information such as ambient temperature. Here we show that the delay of germination 1 (DOG1) gene, known for providing dormancy adaptation to distinct environments, determines the optimal temperature for seed germination. By reciprocal gene-swapping experiments between Brassicaceae species we show that the DOG1-mediated dormancy mechanism is conserved. Biomechanical analyses show that this mechanism regulates the material properties of the endosperm, a seed tissue layer acting as germination barrier to control coat dormancy. We found that DOG1 inhibits the expression of gibberellin (GA)-regulated genes encoding cell-wall remodeling proteins in a temperature-dependent manner. Furthermore we demonstrate that DOG1 causes temperature-dependent alterations in the seed GA metabolism. These alterations in hormone metabolism are brought about by the temperature-dependent differential expression of genes encoding key enzymes of the GA biosynthetic pathway. These effects of DOG1 lead to a temperature-dependent control of endosperm weakening and determine the optimal temperature for germination. The conserved DOG1-mediated coat-dormancy mechanism provides a highly adaptable temperature-sensing mechanism to control the timing of germination.
Department of Botany Faculty of Biology University of Osnabrück D 49069 Osnabrück Germany
Institute for Phytomedicine Geisenheim University D 65366 Geisenheim Germany
Plant Genetics and Cytogenetics Wageningen University NL 6708 Wageningen The Netherlands
References provided by Crossref.org
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- $a Graeber, Kai $u School of Biological Sciences, Plant Molecular Science and Centre for Systems and Synthetic Biology, Royal Holloway, University of London, Egham, Surrey TW20 0EX, United Kingdom; Faculty of Biology, Institute for Biology II, Botany/Plant Physiology, University of Freiburg, D-79104 Freiburg, Germany;
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- $a Seed germination is an important life-cycle transition because it determines subsequent plant survival and reproductive success. To detect optimal spatiotemporal conditions for germination, seeds act as sophisticated environmental sensors integrating information such as ambient temperature. Here we show that the delay of germination 1 (DOG1) gene, known for providing dormancy adaptation to distinct environments, determines the optimal temperature for seed germination. By reciprocal gene-swapping experiments between Brassicaceae species we show that the DOG1-mediated dormancy mechanism is conserved. Biomechanical analyses show that this mechanism regulates the material properties of the endosperm, a seed tissue layer acting as germination barrier to control coat dormancy. We found that DOG1 inhibits the expression of gibberellin (GA)-regulated genes encoding cell-wall remodeling proteins in a temperature-dependent manner. Furthermore we demonstrate that DOG1 causes temperature-dependent alterations in the seed GA metabolism. These alterations in hormone metabolism are brought about by the temperature-dependent differential expression of genes encoding key enzymes of the GA biosynthetic pathway. These effects of DOG1 lead to a temperature-dependent control of endosperm weakening and determine the optimal temperature for germination. The conserved DOG1-mediated coat-dormancy mechanism provides a highly adaptable temperature-sensing mechanism to control the timing of germination.
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- $a Linkies, Ada $u Faculty of Biology, Institute for Biology II, Botany/Plant Physiology, University of Freiburg, D-79104 Freiburg, Germany; Institute for Phytomedicine, Geisenheim University, D-65366 Geisenheim, Germany;
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