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  Species-wide Genetic Incompatibility Analysis Identifies Immune Genes as Hot Spots of Deleterious Epistasis

Chae, E., Bomblies, K., Kim, S.-T., Karelina, D., Zaidem, M., Ossowski, S., et al. (2014). Species-wide Genetic Incompatibility Analysis Identifies Immune Genes as Hot Spots of Deleterious Epistasis. Cell, 159(6), 1341-1351. doi:10.1016/j.cell.2014.10.049.

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 Creators:
Chae, E1, Author           
Bomblies, K1, Author           
Kim, S-T1, Author           
Karelina, D1, Author           
Zaidem, M1, Author           
Ossowski, S1, Author           
Martín-Pizarro, C1, Author           
Laitinen, RAE1, Author           
Rowan, BA1, Author           
Tenenboim, H1, Author           
Lechner, S1, Author           
Demar, M1, Author           
Habring-Müller, A1, Author           
Lanz, C1, Author           
Rätsch, G, Author           
Weigel, D1, Author           
Affiliations:
1Department Molecular Biology, Max Planck Institute for Developmental Biology, Max Planck Society, ou_3375790              

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 Abstract: Intraspecific genetic incompatibilities prevent the assembly of specific alleles into single genotypes and influence genome- and species-wide patterns of sequence variation. A common incompatibility in plants is hybrid necrosis, characterized by autoimmune responses due to epistatic interactions between natural genetic variants. By systematically testing thousands of F1 hybrids of Arabidopsis thaliana strains, we identified a small number of incompatibility hot spots in the genome, often in regions densely populated by nucleotide-binding domain and leucine-rich repeat (NLR) immune receptor genes. In several cases, these immune receptor loci interact with each other, suggestive of conflict within the immune system. A particularly dangerous locus is a highly variable cluster of NLR genes, DM2, which causes multiple independent incompatibilities with genes that encode a range of biochemical functions, including NLRs. Our findings suggest that deleterious interactions of immune receptors limit the combinations of favorable disease resistance alleles accessible to plant genomes.

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Language(s): eng - English
 Dates: 2014-12
 Publication Status: Issued
 Pages: -
 Publishing info: -
 Table of Contents: -
 Rev. Type: -
 Identifiers: DOI: 10.1016/j.cell.2014.10.049
PMC: 25467443
 Degree: -

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Title: Cell
Source Genre: Journal
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Publ. Info: Cambridge, Mass. : Cell Press
Pages: - Volume / Issue: 159 (6) Sequence Number: - Start / End Page: 1341 - 1351 Identifier: ISSN: 0092-8674
CoNE: https://pure.mpg.de/cone/journals/resource/954925463183