Format

Send to

Choose Destination
Cell. 2014 Dec 4;159(6):1341-51. doi: 10.1016/j.cell.2014.10.049. Epub 2014 Nov 20.

Species-wide genetic incompatibility analysis identifies immune genes as hot spots of deleterious epistasis.

Author information

1
Department of Molecular Biology, Max Planck Institute for Developmental Biology, 72076 Tübingen, Germany.
2
Department of Molecular Biology, Max Planck Institute for Developmental Biology, 72076 Tübingen, Germany; Friedrich Miescher Laboratory, Max Planck Society, 72076 Tübingen, Germany.
3
Friedrich Miescher Laboratory, Max Planck Society, 72076 Tübingen, Germany.
4
Department of Molecular Biology, Max Planck Institute for Developmental Biology, 72076 Tübingen, Germany. Electronic address: weigel@weigelworld.org.

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.

PMID:
25467443
PMCID:
PMC4269942
DOI:
10.1016/j.cell.2014.10.049
[Indexed for MEDLINE]
Free PMC Article

Supplemental Content

Full text links

Icon for Elsevier Science Icon for PubMed Central
Loading ...
Support Center