The AVR9 peptide of the fungal pathogen Cladosporium fulvum and the INF1 protein of the oomycete pathogen Phytophthora infestans elicit the hypersensitive response (HR) on Cf9 tomato or Cf-9 transgenic tobacco and on all cultivars of tobacco, respectively. Expression of either the functional Avr9 or inf1 genes from engineered potato virus X (PVX) genomes resulted in localized HR lesions on tobacco plants responsive to the elicitors and inhibited spread of the recombinant virus. In contrast, PVX derivatives producing mutant forms of AVR9 and INF1 with reduced elicitor activity caused systemic necrotic and/or mosaic symptoms, and were unable to inhibit PVX spread. These results demonstrate that HR is a highly versatile defense mechanism active against unrelated pathogens irrespective of the HR-inducing agent, and that resistance to recombinant PVX in tobacco is correlated with the strength of the transgene-encoded elicitor.

Thirty-six populations of the potato cyst nematodeGlobodera pallida, all collected in the Netherlands, were analysed twice: by two-dimensional gel electrophoresis of proteins (2-DGE) and by random amplified polymorphic DNA fingerprinting (RAPD). Two-DGE revealed frequencies of 21 alleles at eight putative loci in each population. The same populations were subjected to RAPD analysis. This qualitative technique revealed 38 polymorphic DNA fragments. Both datasets were independently processed to determine the intraspecific variation. UPGMA analysis resulted in a 2-DGE- and a RAPD-based dendrogram with cophenetic correlation coefficients of 0.755 and 0.838 respectively. The correlation between the genetic similarity values for the populations was 0.572. Comparison between the 2-DGE- and the RAPD-based dendrogram revealed that only thirteen of the 36 populations analysed were clustered identically. It is concluded that the gene pool similarity concept is only in some instances applicable to Dutch populations ofG. pallida. For populations that could not be differentiated unequivocally on the basis of molecular markers, markers closely linked to avirulence genes should be identified. Approaches that will lead to the identification of such markers are discussed.