한빛사 논문
Eunyoung Chae1, Kirsten Bomblies1, 3, Sang-Tae Kim1, 4, Darya Karelina1, 2, Maricris Zaidem1, Stephan Ossowski1, 5, Carmen Martin-Pizarro1, Roosa A.E. Laitinen1, 6, Beth A. Rowan1, Hezi Tenenboim1, 6, Sarah Lechner1, 7, Monika Demar1, Anette Habring-Muller1, Christa Lanz1, Gunnar Ratsch2, 8, Detlef Weigel1
1 Department of Molecular Biology, Max Planck Institute for Developmental Biology, 72076 Tubingen, Germany
2 Friedrich Miescher Laboratory, Max Planck Society, 72076 Tubingen, Germany
3 Present address: Department of Organismic and Evolutionary Biology, Harvard University, Cambridge, MA 02138, USA
4 Present address: Center for Genome Engineering, Institute for Basic Science, 305-811 Daejeon, South Korea
5 Present address: Genomic and Epigenomic Variation in Disease Group, Centre for Genomic Regulation and Universitat Pompeu Fabra, 08003 Barcelona, Spain
6 Present address: Max Planck Institute of Molecular Plant Physiology, 14476 Potsdam-Golm, Germany
7 Present address: CeGAT GmbH, 72076 Tubingen, Germany
8 Present address: Computational Biology Center, Memorial Sloan Kettering Cancer Center, New York, NY 10065, USA
Corresponding author : Detlef Weigel
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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