Resistance to the root-knot nematode Meloidogyne fallax in Solanum sparsipilum: analysis of the mechanisms

The genotype 88S.329.15 of Solanum sparsipilum was studied in order to analyse the genetic basis and the mechanisms of its resistance to Meloidogyne fallax. In infected plants grown at 20°C, juveniles invaded the root system with a clear delay and a lower infection rate in comparison to the susceptible S. tuberosum genotype BF15 H1. No defence reaction occurred during root invasion and migration toward the vascular cylinder. The juveniles induced development of feeding sites usually composed of several giant cells, which contained condensed cytoplasm, only small vacuoles, enlarged nuclei with pronounced nucleoli and almost no endoplasmic reticulum. Abundant necrosis of surrounding parenchymatous vascular cylinder cells lead to the degeneration of the giant cells. More than 90% of the invading juveniles failed to develop. The others developed as males. The resistance inheritance was analysed on 128 F1 hybrids obtained using the susceptible line BF15 H1 as the female parent and 88S.329.15 as the male parent. Among the progenies, 68 genotypes produced a necrotic reaction to nematode infection and 60 produced no necrosis. This 1 : 1 segregation pattern suggests a monogenic control of this defence reaction. Unlike the resistant parent 88S.329.15, some M. fallax females developed in the roots of necrotically responding hybrids. There was a normal distribution of mean numbers of adult females found in the roots of these genotypes. This result suggests that the ability of the resistant genotype 88S.329.15 to suppress development of females is quantitatively inherited and likely to be controlled by more than one locus. These data indicate that the mechanism of resistance is different from the resistance to Meloidogyne incognita conferred by the Mi gene of tomato.