Epidermal cell monolayers prepared from partially dissected barley (Hordeum vulgare) coleoptiles were used for in vivo analysis of race-specific resistance to powdery mildew (Erysiphe graminis f. sp. hordei) specified by host genes Mla-1, Mla-12, and Mlg. Complete resistance governed by each of these genes is closely associated with hypersensitive cell death (hypersensitive response, HR) in primary leaf tissue. In contrast, Mla-12 coleoptile tissue reveals a fully compatible, Mla-1 coleoptile tissue a partially compatible, and Mlg coleoptile tissue an incompatible interaction upon challenge with pathogen races carrying corresponding avirulence functions. Quantitative recording of single plant-fungus interaction sites showed arrest of fungal development in papillae on Mlg coleoptiles. On Mla-1 and Mla-12 coleoptiles, attacked cells become predominantly penetrated by the fungus. Approximately one third of penetrated cells on Mla-1 coleoptiles subsequently undergo an HR. These sites reveal no further fungal development. Both Mlg and Mla-12 coleoptiles fail to mount an HR. The effect of cordycepin (3′-deoxyadenosine), an inhibitor of mRNA synthesis, was studied in planta on primary leaf tissue of Mla-12 and Mlg genotypes. Host cell death triggered by either gene is reduced to background levels observed in the near-isogenic compatible interaction and exhibits the same dose-dependent cordycepin sensitivity. Inhibition of Mlg-triggered, single-cell HR is not accompanied by release of fungal growth arrest, indicating cordycepin insensitivity of a papillae-associated resistance component. The data suggest that host cell death is a requisite component for expression of Mla-type but not Mlg-type resistance.

The identification of a variety has an important role in the protection of plant breeders' rights and for monitoring seed production and marketing. The objective of our study was to examine whether or not a large number of registered cultivars of European potato (Solarium tuberosum subsp, tuberosum) could be distinguished using RFLPs (restriction fragment length polymorphisms) as genetic fingerprints. Genomic Southern blots with TaqI‐restricted DNA of 136 tetraploid potato varieties were hybridized to highly polymorphic potato RFLP markers. The use of four markers was sufficient to identify 130 of 136 varieties. Three pairs of varieties were identical with all markers evaluated. One marker, GP35, was the most effective: out of 134 varieties analyzed with this probe, 122 had unique RFLP patterns. The remaining 12 varieties were divided into six pairs, each showing an identical pattern. Sequence analysis showed that GP35 was not homologous to minisatellite sequences. The probability of finding a random match of RFLP patterns between two tetraploid varieties with marker GP35 was estimated to be 0.63 × 10−4. Variety identification by RFLP fingerprints is therefore feasible in potato.

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SummaryThe semi‐dominantly acting allele of the Mlg locus in barley confers a race‐specific resistance to the causal agent of powdery mildew, Erysiphe graminis f.sp. hordei. High resolution genetic mapping via RFLP analysis enabled us to identify a set of markers on chromosome 4 which are either tightly linked or co‐segregate with the resistance function. Comparison of marker distances in segregating F2 populations originating from different genotypes revealed an unex‐pected variation of recombination frequencies in the vicinity of the locus. Based on near‐isogenic lines carrying either resistance gene Mlg or Mla12 and a cell‐type specific analysis it was demonstrated that Mlg acts at an earlier stage of fungal development than Mla12. A time‐course analysis of the early infection process combined with gene dosage experiments provided strong evidence that attacked cells retain viability after the defence response and that hypersensitive cell death (HR) is a secondary consequence, but not causally required for Mlg‐mediated arrest of fungal growth. It is speculated that gene dosage experiments may provide a means to separate primary from secondary defence reactions.

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