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Arabidopsis thaliana: A Plant as a Model for Human Disease

Arabidopsis thaliana has a long history as a laboratory plant owing to its small size (10 cm) and relatively short life cycle (about 6 weeks from germination to mature seed; for details see http://www.arabidopsis.org). This flowering plant, which belongs to the Brassicaceae family, was established as a model for all higher plants in the early 1980s. Compared to many other plants it has a very small genome (120 Mbp). The analysis of the genome resulted in the prediction of more than 24000 genes [8]. Furthermore, a collection of mutant strains is available that covers about three-quarters of the genome [9].

At first glance, to take a plant as model for human infectious diseases seems ridiculous. However, A. thaliana contains numerous genes similar to those related to human diseases ranging from cancer and premature aging. Moreover, the fact that some broad-host-range pathogens such as Pseudomonas spp. are able to infect plants as well as animals led to the conclusion that at least parts of the attacking strategies are the same for all host organisms. On the host side, there seem to be larger differences in defense strategies. Whereas plants recognize specific effectors of the pathogen, animals can sense molecular patterns [10] that differ between pathogen species. Generally, plant pathogens do not enter the host cells, but occupy the intercellular spaces in leaves by entering the natural leave openings, the stomata. Many bacteria then activate the Hrp-locus genes, which encode for a type III secretion system [11]. This secretion system then is used to inject virulence effector proteins into the plant cell. These effectors are specifically recognized by the plant cell through LRR-containing proteins (NB-LRR), which in turn activate a signal transduction cascade to trigger the host response. Animals use also LRR-containing molecules as receptors, albeit with different specificities and different additional domains [10]. Thus, whereas the plant-pathogen interaction model can tell us much about the strategies a pathogen uses for infection, the host factors responsible for susceptibility and resistance differ between the eukaryote kingdoms.

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