Gurmel S. Sidhu

The use of amino acid fungal auxotrophs to study the predisposition phenomena in the root-knot-wilt fungus disease complex of tomato

Abstract Root-knot nematode ( Meloidogyne incognita ) infections of tomato plants resistant to the wilt fungus ( Fusarium oxysporum f. sp. lycopersici ) often predispose the tomato to this fungus. The role of free amino acids, which are abundant in nematode-galled tissue, in the predisposition of a resistant host to the fungus was investigated. Amino acid levels in the exudates of healthy and nematode-galled tomato cultivars were determined. Single step amino acid mutants (auxotrophs) were induced in the wild type (race 1) wilt fungus. Those auxotrophs that lost their relative pathogenicity as compared to the wild type were selected for the study of the influence of increased or decreased levels of the corresponding free amino acids in the exudates of host cultivars. Auxotrophs requiring threonine, proline, methionine, histidine and glycine were pathogenic only when the relevant amino acid was present above a certain threshold level in the exudates of genetically susceptible, nematode-galled cultivars. However, these caused negligible pathogenicity in nematode-inoculated cultivars that are genetically fungal resistant. A similar trend in pathogenicity was observed when threonine, proline, methionine and histidine were applied exogenously to the tomato cultivars before inoculation with the fungal auxotrophs. The role of these and other amino acid auxotrophs are discussed in the light of the nutritional hypotheses of Lewis and Garber [ 12, 18 ]. These experiments show that amino acids may play a significant role in predisposing fungal-resistant plants in a disease complex.

Predisposition of Tomato To the Wilt Fungus (Fusarium Oxysporum Lycopersici) By the Root-Knot Nematode (Meloidogyne Incognita)

Root-knot nematodes (Meloidogyne incognita) often occur together with the wilt fungus (Fusarium oxysporum f. lycopersici) on tomato in a plant disease complex. An interaction between the plant and the nematode may transform a genetically resistant host plant into one that is susceptible to the wilt-fungus and which subsequently develops wilt symptoms. Bridging and grafting experiments indicate that a factor emanating from this nematode-plant interaction is translocated considerable distances to the upper foliage across a resistant scion. Disease indices based on chlorosis of the foliage and on propagule counts from stem exudates showed primarily distal rather than proximal translocation of the factor.

Genetic Control of Resistance in Tomato I. Identification of Genes for Host Resistance To Meloidogyne Incognita

The genetic control of resistance and susceptibility of seven tomato cultivars was investigated against a single stock culture of Meloidogyne incognita. Segregations obtained from the F 2 and backcross progenies derived from crosses Nematex X Chico III, Nematex X Enterprizer, Small Fry X Chesapeake, and Cold Set X IPB show that the cultivars Nematex, Small Fry, and Cold Set each possess a single gene for resistance. The resistance gene was dominant in cultivars Nematex and Small Fry and recessive in cultivar Cold Set. The three R-genes possessed by cultivars Nematex, Small Fry, and Cold Set are tentatively designated as LMiR 1 , LMiR 2 , and LMir 3 , respectively.

Genetics of tomato resistance to the Fusarium-Verficillium complex

Abstract In the Fusarium-Verticillium wilt disease complex on tomato, Fusarium-resistant tomato cultivars become relatively resistant to Verticillium. This induction of resistance by Fusarium oxysporum f. sp. lycopersici (F) against Verticillium albo-atrum (V) was evaluated genetically by testing F1, F2 and testcross progenies derived from VFN-8 × Bonny Best tomato cross. The segregating progenies were tested singly (F or V) and simultaneously (F+V). Two independent dominant genes for resistance were identified—one effective against Fusarium race 1 (FIR1) and the other against Verticillium (VaR1). Fusarium-resistant but Verticillium-susceptible tomato genotypes also exhibited a resistance response to Verticillium when tested simultaneously with both fungal pathogens. As a result, the dihybrid ratio (9 : 3 : 3 : 1) observed from single infections (i.e. F or V) was modified to an epistatic ratio 12 : 3 : 1 corresponding to resistance to both, to one or to none of the two pathogens, respectively. This ratio is characteristic of dominant epistasis. Implications of such genetic modifications in disease complexes for plant breeding are discussed.