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Abstract:
A survey of the F1 offspring of 1487 crosses in Arabidopsis revealed 25 F1 hybrid necrosis cases. These include at least 5 genetically independent systems that we are currently analysing. The first gene underlying hybrid incompatibility that has been cloned turned out to be a homolog of NB-LRR R-genes, a gene class involved in disease resistance in plants (Bomblies et al 2007). Together with expression profiling and presence of cell death it was concluded that several of the hybrids suffer from autoimmunity. Interestingly, despite most of the cases involving 2-3 loci, as the basic Dobzhansky-Muller model assumes, there are some cases in which the genetic incompatibility seems to be due to heterozygous disadvantage at a single locus. I will present one such case, which appears to be responsible for incompatibility in several crosses. Other alleles at this locus cause necrotic lesions in inbred strains, providing a connection between incompatibility between strains and potential fitness trade-offs within strains. To further explore the genetic land-scape leading to hybrid weakness, we have screened F2 populations for recessive incompatibilities. I will present a situation where F2 plants are small and purple, while F1 plants have an altered inflorescence habit. The F1 and F2 phenotypes are linked and map to two epistatically acting loci. Hybrid weakness is found in many flowering plants and could lead to reproductive barriers within populations. Using Arabidopsis thaliana as a model system we are able to illuminate the very early steps of divergence when species are not yet separated.
