We present a model pathosystem to dissect genetically the disease resistance response of plants against phytopathogenic bacteria. The interaction between Pseudomonas syringae pathovar maculicola (Psm) and Arabidopsis thaliana displays phenotypic varia-ion which depends on the genotype of both partners. Compatible interactions are defined by sustained in-planta bacterial growth and are normally accompanied of their appearance. For compatible interactions, resistance is defined by limited in-planta bacterial growth accompanied by a typical 'hypersensitive response' (HR). We show that at least parts of this system fit the paradigms of Flor's 'gene-for-gene' hypothesis. We identify functionally a putative bacterial avirulence gene (avrRpm 1) from a Psm isolate which conditions the HR on A. thaliana ecotypes Oy-0 abd Col- 0, but not Nd-0. We also demonstrate that resistance to the Psm strain from which avrRpm1 was isolated segregates as a single trait in the crosses Col-o x Nd-0 and Nd-0 x Oy-0. Furthermore, we map this locus (RPM1) molecularly in the Col-0 x Nd-0 cross to a relatively small interval defined by two RFLP markers on A. thliana chromosome 3. Resistance in the second cross also maps to this locus and co-segregates with resistance to avrRpm1.
Seven races of Rhynchosporium secalis were screened for their virulence on a variety of barley cultivars. Four races were identified as virulent on cultivar Atlas 46 (resistance loci Rrs1 and Rrs2) but virulent on the near-isogenic cultivar Atlas (Rrs2). For one of these races, US238.1, the fungal infection cycle was followed on the susceptible cultivar by means of light and scanning electron microscopy. From a comparative analysis of fungal development on the susceptible and resistant cultivars, two lines of plant defense emerged: (i) inhibition of spore germination on the leaf surface and (ii) prevention of the establishment of the subcuticular stroma. Investigations of the development of race US238.1 on different barley cultivars with and without Rrs1 and on F1 individuals from different crosses excluded involvement of Rrs1 in the inhibition of spore germination. Possible pathogenicity mechanisms are discussed. Key words: leaf scald, microscopy, plant resistance.
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