An Integrated Management Strategy for Bacterial Speck Disease of Tomato in New York: Deciphering the Web of Induced Resistance

Abstract

Incorporating plant activators into integrative pest management programs is an appealing option for controlling bacterial diseases of greenhouse and field-grown tomatoes. Two types of plant activators, compounds that control disease without directly impacting pathogens, were evaluated for effects on tomato defense gene activation, disease control and yield. The two plant activators involve different signaling pathways; one induces systemic acquired resistance (SAR) and a second activates induced systemic resistance (ISR). In greenhouse assays, acibenzolar-S-methyl (ASM, SAR-inducing compound) effectively reduced bacterial speck incidence and severity, both alone and with the ISR-inducing compound (mixture of two Bacillus spp. known as plant growth-promoting rhizobacteria, PGPR). Elevated activation of salicylic acid (SA) and ethylene (ET) pathways was observed following ASM application. The PGPR compound provided inadequate disease control and inconsistently modified defense gene expression. Combining the two activators did not involve negative cross-talk between signaling pathways as disease control was on par with or better than ASM alone. Based on these results, ASM appears to be a viable option for bacterial speck management in greenhouse tomato transplant production. Defense gene activation in three field-grown tomato cultivars via ASM was evaluated without pathogen pressure. Quantitative real-time PCR analysis following two ASM applications revealed that ASM induced the SA and ET, but not jasmonic acid (JA), pathways in all cultivars tested. Gene expression in all three cultivars responded with higher activation following the second ASM application (applied seven days after the first). ASM, PGPR and copper were evaluated for control of bacterial speck and tomato defense gene activation over three field seasons. ASM controlled Pseudomonas syringae pv. tomato as well as copper with no negative effect on yield. The PGPR compound reduced bacterial speck symptoms though provided inconsistent control and no priming of signaling pathways was observed. Alone or in combination with ASM, the PGPR compound provided some yield boost in one of three years. All treatments negatively impacted pathogen growth. Response of ASM-treated plants was dependant on disease pressure; SA and ET pathways were activated to detectable levels only under high disease pressure. Implications of these findings on management strategies and defense pathway interactions are discussed.