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  Autoimmune response as a mechanism for a Dobzhansky-Muller-type incompatibility syndrome in plants

Bomblies, K., Lempe, J., Epple, P., Warthmann, N., Lanz, C., Dangl, J., et al. (2007). Autoimmune response as a mechanism for a Dobzhansky-Muller-type incompatibility syndrome in plants. PLoS Biology, 5(9): e236. doi:10.1371/journal.pbio.0050236.

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Bomblies, K1, Autor           
Lempe, J1, Autor           
Epple, P, Autor
Warthmann, N1, Autor           
Lanz, C1, Autor           
Dangl, JL, Autor
Weigel, D1, Autor           
Affiliations:
1Department Molecular Biology, Max Planck Institute for Developmental Biology, Max Planck Society, ou_3375790              

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 Zusammenfassung: Epistatic interactions between genes are a major factor in evolution. Hybrid necrosis is an example of a deleterious phenotype caused by epistatic interactions that is observed in many intra- and interspecific plant hybrids. A large number of hybrid necrosis cases share phenotypic similarities, suggesting a common underlying mechanism across a wide range of plant species. Here, we report that approximately 2% of intraspecific crosses in Arabidopsis thaliana yield F1 progeny that express necrosis when grown under conditions typical of their natural habitats. We show that several independent cases result from epistatic interactions that trigger autoimmune-like responses. In at least one case, an allele of an NB-LRR disease resistance gene homolog is both necessary and sufficient for the induction of hybrid necrosis, when combined with a specific allele at a second locus. The A. thaliana cases provide insights into the molecular causes of hybrid necrosis, and serve as a model for further investigation of intra- and interspecific incompatibilities caused by a simple epistatic interaction. Moreover, our finding that plant immune-system genes are involved in hybrid necrosis suggests that selective pressures related to host-pathogen conflict might cause the evolution of gene flow barriers in plants.

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 Datum: 2007-09
 Publikationsstatus: Erschienen
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 Ort, Verlag, Ausgabe: -
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 Art der Begutachtung: -
 Identifikatoren: DOI: 10.1371/journal.pbio.0050236
PMID: 17803357
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Titel: PLoS Biology
  Andere : PLoS Biol.
Genre der Quelle: Zeitschrift
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Ort, Verlag, Ausgabe: San Francisco, California, US : Public Library of Science
Seiten: 11 Band / Heft: 5 (9) Artikelnummer: e236 Start- / Endseite: - Identifikator: ISSN: 1544-9173
CoNE: https://pure.mpg.de/cone/journals/resource/111056649444170