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

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 Abstract: 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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 Dates: 2007-09
 Publication Status: Issued
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 Rev. Type: -
 Identifiers: DOI: 10.1371/journal.pbio.0050236
PMID: 17803357
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Title: PLoS Biology
  Other : PLoS Biol.
Source Genre: Journal
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Publ. Info: San Francisco, California, US : Public Library of Science
Pages: 11 Volume / Issue: 5 (9) Sequence Number: e236 Start / End Page: - Identifier: ISSN: 1544-9173
CoNE: https://pure.mpg.de/cone/journals/resource/111056649444170