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Two-locus F1 hybrid incompatibility of two wild Arabidopsis thaliana ecotypes

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Bomblies,  K       
Department Molecular Biology, Max Planck Institute for Developmental Biology, Max Planck Society;

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Lempe,  J       
Department Molecular Biology, Max Planck Institute for Developmental Biology, Max Planck Society;

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Weigel,  D       
Department Molecular Biology, Max Planck Institute for Developmental Biology, Max Planck Society;

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引用

Bomblies, K., Lempe, J., & Weigel, D. (2005). Two-locus F1 hybrid incompatibility of two wild Arabidopsis thaliana ecotypes. Poster presented at 16th International Conference on Arabidopsis Research (ICAR 2005), Madison, WI, USA.


引用: https://hdl.handle.net/21.11116/0000-000C-2243-2
要旨
Postzygotic hybrid incompatibility is a commonly observed type of reproductive isolation, which is a defining step in both animal and plant speciation. How hybrid incompatibility can arise in the first place presents a theoretical difficulty: by definition, mutations leading to infertile or unfit progeny are mal-adaptive. A potential solution to this problem is described by the Dobzhansky-Muller model, which posits that two (or more) genes evolve independently in individuals or populations that do not interbreed. Although not detrimental in their native genomic context, when combined through hybridization, the differently evolved gene pairs interact to cause lethality or sterility. We have identified a temperature sensitive incompatibility between two wild Arabidopsis ecotypes, Uk-1 and Uk-3, whose F1 and F2 segregation conforms to the expectations for a two-locus Dobzhansky-Muller type mechanism. The genetic incompatibility is dominant, but specific; crosses of either ecotype with a panel of 20 other ecotypes produce normal progeny. Uk-1/Uk-3 hybrid plants are normal at 23°C, but at 16°C (which is more representative of where Uk-1 and Uk-3 were collected), F1 plants show severe progressive growth arrest and only rarely produce flowers, which are infertile. Widespread cell death is observed in F1 leaves and correlates with severity of the phenotype. An additional seedling lethal phenotype is observed in the F2 and is associated with early-onset cell death in the meristem. We performed micro-array analysis on F1 and parent plants shifted from 23°C to 16°C to investigate the physiology underlying the F1 defects. The suite of genes differentially expressed in F1 progeny (but not in parents) at 16°C includes many genes with known or predicted roles in pathogen response. This suggests that an aberrant interaction of Uk-1 and Uk-3-derived genes involved in disease resistance signaling triggers a constitutive disease response, culminating in extensive cell death and growth defects. Preliminary mapping and genotype/phenotype associations suggest that the incompatibility is caused by interaction of one region on chromosome 3 from Uk-1, and one region on chromosome 5 from Uk-3. We are currently fine mapping the causative genes. Cloning of these genes will represent the first molecular identification of a gene pair involved in Dobzhansky-Muller type genetic isolation in plants, and provides a mechanistic model of how reproductive isolation can arise within a plant species.