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Resistance in Lycopersicon esculentum var. cerasiforme to Cladosporium fulvum

Gallo, M., Ciccarese, F., Jaupi, M.
Acta horticulturae 2012 no.960 pp. 77-82
Fulvia fulva, Oidium neolycopersici, Solanum lycopersicum var. cerasiforme, Solanum pimpinellifolium, conidia, conidiophores, cultivars, disease control, dominant genes, economics, fungi, genotype, germ tube, germination, greenhouses, hypersensitive response, leaves, models, necrosis, recessive genes, screening, sporulation, tomatoes
Leaf mould caused by Cladosporium fulvum is one of the most widespread tomato disease in greenhouse. The use of resistant cultivars is the most economic and decisive tool to control the disease. In a screening for leaf mould resistance numerous accessions of Lycopersicon pimpinellifolium, L. peruvianum and L. esculentum var. cerasiforme and the race 0 of C. fulvum were used. Among the tested accessions a general reaction of susceptibility was observed. Only the one accession of L. esculentum var. cerasiforme was resistant to C. fulvum. This accession was self-fertilized and signed as line R-28. The resistance reaction was evident on leaves with chlorotic spots that later became necrotic. Microscopic observations showed no differences between the resistant and the susceptible genotypes either in the phase of conidia germination and in elongation of germ tube. After one week on the susceptible plants conidiophores were evident whereas, on the leaves of line R-28 accession, fungi sporulation was never observed. In inheritance analysis, segregation ratios strongly fitted a single and dominant gene model conferring resistance in line R-28. Necrosis of leaves indicated that the resistance mechanism was a hypersensitive reaction. Resistance to C. fulvum found in the accession line R-28 is the first report about a monogenic and dominant gene in L. esculentum var. cerasiforme. It is important to emphasize that in previous studies in the accession line R-28 were also identified a resistance to Oidium neolycopersici conferred by a single recessive gene signed as ol-2.