Polygenic Resistance Of Tomato Plants To Fusarium Oxysporum Fsp Lycopersici

Fusarium oxysporum causes vascular wilt disease in a broad range of crops, including tomato (Solanum lycopersicum). Tomato, a major and important vegetable crop, is susceptible to F. oxysporum f. sp. lycopersici (FOL), a biotrophic pathogen that is the causal agent of tomato wilt resulting in significant yield losses each year. Development of disease in susceptible tomato plants requires FOL to advance through a series of transitions, beginning with spore germination and culminating with establishment of a systemic infection. In addition, many host attributes, including the composition of root exudates, the structure of the root cortex, and the capacity to recognize and respond quickly to invasive growth of a pathogen, can impede the development of FOL. FOL divides into races on the basis of the ability of individual strains to overcome specific genes. This implies the presence of avirulence genes (Avr) in the fungus that is recognized by products of the corresponding genes. In tomato, resistance (R) genes against the wilt-inducing FOL are called immunity genes, and the interaction between these genes will determine the success of the infection.

Bioassays of acetone extracts from xylem tissue in tomato stems and corresponding reductions in Fusarium oxysporum f.sp. lycopersici race 1 or 2 populations within the stems suggest that fungitoxic materials within the xylem vessels of Bonny Best, Jefferson, and Marglobe tomato cultivars initially kill a portion of the inoculum conidia. In the susceptible host-pathogen combinations, the pathogen eventually grows extensively in the xylem vessels and severe disease symptoms follow closely the proliferation of the pathogen. Acetone extracts from the susceptible Bonny Best cultivar do not become highly fungitoxic until eight or nine days after inoculation when the disease symptoms are already severe. Xylem extracts from the multigenic resistant Marglobe, however, do not become fungitoxic, even 11 days after inoculation with race 1 of the pathogen when the disease symptoms are severe and the Fusarium population is seven times that in Bonny Best-race 1 inoculated plants. In the monogenic resistant Jefferson-race 1 combination, within three to four days after inoculation the xylem extracts become highly fungitoxic, the fungal population within the stem remains low and disease symptoms fail to develop. The xylem extracts from race 1 resistant Jefferson inoculated with race 2 of the pathogen do not become fungitoxic even when disease symptoms are exhibited and the Fusarium population has reached a peak nearly three times that in Bonny Best-race 1 inoculated plants. Conidia of race 2 were as sensitive to the xylem toxicants produced in response to infection by race 1 as were race 1 conidia. The breaking of Fusarium wilt resistance by race 2 of the pathogen may be a result of this race's failure to induce the production or release of fungitoxic materials in the xylem of Jefferson in response to infection and is not due to resistance of race 2 to toxicants in Jefferson. Xylem vessels in stems of Jefferson (race 1 resistant and race 2 susceptible) and Bonny Best (race 1 susceptible) tomato cultivars inoculated with Fusarium oxysporum f.sp. lycopersici race 1 or 2 were examined by scanning electron microscopy. Four days after inoculation of Jefferson with race 1 conidia, the inoculum conidia and resultant hyphae were collapsed, while in the susceptible host-pathogen combinations the conidia and hyphae appeared normal. Vessel elements of both resistant and susceptible host-pathogen combinations had no perforation plates or tyloses capable of trapping conidia or effectively blocking hyphal growth within the vessel elements. Perforation plates are reduced to slightly lipped rims at the ends of vessel elements thereby providing an unrestricted aperature for hyphal growth and conidial movement in the transpiration stream. In the susceptible host-pathogen combinations, mycelial growth often filled vessel lumens, but no sporulation was noted. Frequent lateral spread of the pathogen occurred from one vessel element to adjacent vessel elements through common pits. The infrequent occurrence of tyloses (in less than 1% of vessel elements) and lack of complete occlusion by tyloses in the resistant host-pathogen combination suggest that vascular wilt resistance is not due to physical containment of the pathogen. Collapsed conidia and hyphae in the resistant Jefferson-race 1 combination may indicate that fungitoxic materials suppress the pathogen and lead to resistance.

Proceedings of the CEC/IOBC Expert's Group Meeting, Pennes, France, November 1985. Forty contributions (authors are from 12 countries and two international organizations) deal with crops such as cabbages, carrots, tomatoes, potatoes, beans, and artichokes and with the particularly urgent task of red