Mechanisms of Action and Dose-Response Relationships Governing Biological Control of Fusarium Wilt of Tomato by NonpathogenicFusariumspp.

Abstract

Three isolates of nonpathogenic Fusarium spp. (CS-1, CS-20, and Fo47), previously shown to reduce the incidence of Fusarium wilt diseases of multiple crops, were evaluated to determine their mechanisms of action and antagonist-pathogen inoculum density relationships. Competition for nutrients, as represented by a reduction in pathogen saprophytic growth in the presence of the biocontrol isolates, was observed to be an important mechanism of action for isolate Fo47, but not for isolates CS-1 and CS-20. All three biocontrol isolates demonstrated some degree of induced systemic resistance in tomato (Lycopersicon esculentum) and watermelon (Citrullus lanatus) plants, as determined by split-root tests, but varied in their relative abilities to reduce disease. Isolate CS-20 provided the most effective control (39 to 53% disease reduction), while Fo47 provided the least effective control (23 to 25% reduction) in split-root tests. Dose-response relationships also differed considerably among the three biocon-trol isolates, with CS-20 significantly reducing disease incidence at antagonist doses as low as 100 chlamydospores per g of soil (cgs) and at pathogen densities up to 10(5) cgs. Isolate CS-1 also was generally effective at antagonist densities of 100 to 5,000 cgs, but only when pathogen densities were below 10(4) cgs. Isolate Fo47 was effective only at antagonist densities of 10(4) to 10(5) cgs, regardless of pathogen density. Epidemiological dose-response models (described by linear, negative exponential, hyperbolic saturation [HS], and logistic [LG] functions) fit to the observed data were used to quantify differences among the biocontrol isolates and establish biocontrol characteristics. Each isolate required a different model to best describe its dose-response characteristics, with the HS/HS, LG/HS, and LG/LG models (pathogen/biocontrol components) providing the best fit for isolates CS-1, CS-20, and Fo47, respectively. Model parameters (defining effective biocontrol dose (ED(50)) indicated an ED(50) of 2.6, 36.3, and 2.1 x 10(6) cgs and estimates of biocontrol efficiency of 0.229, 0.539, and 0.774 for isolates CS-1, CS-20, and Fo47, respectively. Differences in dose-response relationships among the biocontrol isolates were attributed to differences in their mechanisms of action, with CS-20 and CS-1 functioning primarily by induced resistance and Fo47 functioning primarily by competition for nutrients.

Isolation and characterization of Fusarium oxysporum, a wilt causing fungus, for its pathogenic and non-pathogenic nature in tomato (Solanum lycopersicum)

“…These isolates caused wilt symptoms on at least one plant while on inoculation of non pathogenic isolates on the tomato plant, wilt did not occur at all. There are reports of nonpathogenic F. oxysporum demonstrating competing for infection sites and for nutrients, and by induction of resistance (Larkin and Fravel 1999;Benhamou and Garand 2001 Rest of the four non pathogenic isolate of F.oxysporum reduced the colony growth of pathogenic F. oxysporum varied to reduce growth from 0% to 50%. It has been observed that antagonistic fungi are specific in their antagonistic activity against specific fungi (Saleem et al 2000).…”

“…), gerbera (Gerbera jamesonii Hook. ), basil (Ocimum basilicum L.), asparagus (Asparagus officinalis L.), eggplant (Solanum melongena L.), carnation (Dianthus canyophyllus L.), watermelon (Citrullus lanatus), tomato (Solanum lycopersicum L.), (Minuto et al, 1995ab;Larkin and Fravel, 1999;He et al, 2002;Reid et al, 2002;Silva and Wagner, 2005) and colonize the plant rhizosphere and roots without inducing any symptoms (Benhamou and Garand, 2001). The non-pathogenic antagonistic F. oxysporum have the same characteristics as pathogenic except that they are not disease causing and hence are important because these organisms can sustain up to the crop duration.…”

Fusarium oxysporum (F221-B) as biocontrol agent against plant pathogenic fungi in vitro and in hydroponics

“…So far, many reports have provided such an evidence of successfully using many strains of non-pathogenic F. oxysporum recovered from either diseased rhizosphere soil or suppressive soil for controlling soil-grown crops Fuchs et al 1997;Duijff et al 1998;Fravel et al 2003) but not in hydroponics. Fo47 is the best known and most effective nonpathogenic strain of F. oxysporum which was isolated from a soil naturally suppressive to Fusarium wilt of tomato and melon in France (Alabouvette 1990;Alabouvette & Couteaudier 1992;Alabouvette et al 1993Alabouvette et al , 1996Alabouvette et al , 1998Larkin & Fravel 1999) and has been extensively studied for the control of Fusarium wilt disease of several vegetables and flower crops such as tomato (Fuchs et al 1997(Fuchs et al , 1999Duijff et al 1998), carnation (Lemancean et al 1992, and flax (Duijff et al 1999).…”

Fusarium oxysporum Protects Douglas-fir (Pseudotsuga menziesii) Seedlings from Root Disease Caused by Fusarium commune

“…If so, prior inoculation of Douglas-fir seedlings with certain non-pathogenic F. oxysporum strains may have restricted F. commune access to roots (e.g., Alabouvette et al, 1993;Fuchs et al, 1999). Induced systematic resistance has been reported in Fusarium (Fuchs et al, 1997;Larkin and Fravel, 1999;Mandeel and Baker, 1991). Perhaps, F. oxysporum Q12 is able to induce systematic resistance more effectively than either F. oxysporum Q76 or N16.…”

“…Moreover, this may be why F. oxysporum Q12 was an effective biocontrol agent when applied to seedlings before exposure to F. commune at the same concentration (i.e., 1:1). Other studies indicated that much higher concentrations of the biocontrol agent (e.g., 10:1 to 100:1 for Fo47) must be present to effectively restrict disease when plants are exposed to the pathogen and biocontrol agent simultaneously (Alabouvette et al, 1993;Bolwerk et al, 2005;Larkin and Fravel, 1999). Biocontrol activities can be attributed to diverse factors, such as antibiosis, competition, induced host resistance, interactions with other microbes, or other mechanisms (Fravel et al, 2003;Hadelsman and Stabb, 1996).…”