A light sphagnum peat mix inoculated with Trichoderma hamatum 382 consistently provided a significant (P = 0.05) degree of protection against bacterial spot of tomato and its pathogen Xanthomonas euvesicatoria 110c compared with the control peat mix, even though this biocontrol agent did not colonize aboveground plant parts. To gain insight into the mechanism by which T. hamatum 382 induced resistance in tomato, high-density oligonucleotide microarrays were used to determine its effect on the expression pattern of 15,925 genes in leaves just before they were inoculated with the pathogen. T. hamatum 382 consistently modulated the expression of genes in tomato leaves. We identified 45 genes to be differentially expressed across the replicated treatments, and 41 of these genes could be assigned to at least one of seven functional categories. T. hamatum 382-induced genes have functions associated with biotic or abiotic stress, as well as RNA, DNA, and protein metabolism. Four extensin and extensin-like proteins were induced. However, besides pathogenesis-related protein 5, the main markers of systemic acquired resistance were not significantly induced. This work showed that T. hamatum 382 actively induces systemic changes in plant physiology and disease resistance through systemic modulation of the expression of stress and metabolism genes.

The ecology of the vegetable leaf surface is important to the survival of enteric pathogens. Understanding changes in ecological parameters during the preharvest stages of production can lead to development of approaches to minimize the hazard of contamination of fresh fruits and vegetables with foodborne pathogens. In this study, survival levels of Escherichia coli O157 over a 10-day period were compared among traumatically injured, phytopathogen-damaged, and healthy lettuce plants. Leaves from lettuce plants cracked along the central vein, plants infected with Xanthomonas campestris pv. vitians, and healthy plants were inoculated with E. coli O157:H7. The presence of E. coli O157:H7 populations on inoculated leaves and non-inoculated leaves of these same plants was determined for 10 days. The density of E. coli O157:H7 decreased over time on the inoculated leaves regardless of the treatment. The population of E. coli O157:H7 remained higher on traumatically injured leaves than on healthy plants (P < 0.001). E. coli O157:H7 was detected on leaves other than the direct inoculation site of the enteric pathogen in all three treatments groups. Preharvest damage, especially that caused by traumatic injury, impacted the survivability of E. coli O157:H7. Maintaining healthy plants and minimizing physical damage around the time of harvest might improve the safety of fresh produce.

We used molecular markers to identify quantitative trait loci (QTL) that confer resistance in the field to Xanthomonas campestris pv. vesicatoria race T1, a causal agent of bacterial spot of tomato. An F(2) population derived from a cross between Hawaii 7998 (H 7998) and an elite breeding line, Ohio 88119, was used for the initial identification of an association between molecular markers and resistance as measured by bacterial populations in individual plants in the greenhouse. Polymorphism in this cross between a Lycopersicon esculentum donor of resistance and an elite L. esculentum parent was limited. The targeted use of a core set of 148 polymerase chain reaction-based markers that were identified as polymorphic in L. esculentum x L. esculentum crosses resulted in the identification of 37 markers that were polymorphic for the cross of interest. Previous studies using an H 7998 x L. pennellii wide cross implicated three loci, Rx1, Rx2, and Rx3, in the hypersensitive response to T1 strains. Markers that we identified were linked to the Rx1 and Rx3 loci, but no markers were identified in the region of chromosome 1 where Rx2 is located. Single marker-trait analysis suggested that chromosome 5, near the Rx3 locus, contributed to reduced bacterial populations in lines carrying the locus from H 7998. The locus on chromosome 5 explained 25% of the phenotypic variation in bacterial populations developing in infected plants. An advanced backcross population and subsequent inbred backcross lines developed using Ohio 88119 as a recurrent parent were used to confirm QTL associations detected in the F(2) population. Markers on chromosome 5 explained 41% of the phenotypic variation for resistance in replicated field trials. In contrast, the Rx1 locus on chromosome 1 did not play a role in resistance to X. campestris pv. vesicatoria race T1 strains as measured by bacterial populations in the greenhouse or symptoms in the field. A locus from H 7998 on chromosome 4 was associated with susceptibility to disease and explained 11% of the total phenotypic variation. Additional variation in resistance was explained by plant maturity (6%), with early maturing families expressing lower levels of resistance, and plant habit (6%), with indeterminate plants displaying more resistance. The markers linked to Rx3 will be useful in selection for resistance in elite x elite crosses.

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