Host adaptation to potato and tomato within the US-1 clonal lineage of Phytophthora infestans in Uganda and Kenya

Twenty isolates of Phytophthora infestans from potato and twenty-two from t omato, collected in Uganda and Kenya in 1995, were compared for dilocus all ozyme genotype, mitochondrial DNA (mtDNA) haplotype, mating type and restri ction fragment length polymorphism (RFLP) fingerprint using probe RG57. Bas ed on RFLP fingerprint and mtDNA haplotype, all isolates were classified in the US-1 clonal lineage. Nonetheless, isolates from potato differed from i solates from tomato in several characteristics. Isolates from potato had th e 86/100 glucose-6-phosphate isomerase (Gpi) genotype, while those from tom ato were 100/100, which represents a variant of US-1 that had been identifi ed previously as US-1.7. Furthermore, while pure cultures of the pathogen w ere acquired from infected potato leaflets by first growing the isolates on potato tuber slices, this approach failed with infected tomato tissue beca use the isolates grew poorly on this medium. Tomato isolates were eventuall y purified using a selective medium. Six isolates from each host were compa red for the diameter of lesions they produced on three tomato and three pot ato cultivars in one or two detached-leaf assays (four isolates from the fi rst test were repeated in the second). On potato leaflets, isolates from po tato caused larger lesions than isolates from tomato. On tomato leaflets, i solates from that host caused larger lesions than did isolates from potato, but the difference was significant in only one test. The interaction betwe en source of inoculum (potato or tomato) and inoculated host (potato or tom ato) was significant in both tests. Isolates from tomato were highly biotro phic on tomato leaflets, producing little or no necrosis during the seven d ays following infection, even though abundant sporulation could be seen. In contrast, isolates from potato sporulated less abundantly on tomato leafle ts and produced darkly pigmented lesions that were most visible on the adax ial side of the leaflets. Nonetheless, all isolates infected and sporulated on both hosts, indicating that host adaptation is not determined by an abi lity to cause disease but rather by quantitative differences in pathogenic fitness. Assessment of Gpi banding patterns, mtDNA haplotype and RFLP finge rprint of 39 isolates from potato collected in Uganda and Kenya in 1997 ind icated that the population had not changed on this host. The population of P. infestans from Kenya and Uganda provides an interesting model for the st udy of quantitative host adaptation.