Bacteria wilt caused by Ralstonia solanacearum has continued to pose a significant threat to a wide range of agricultural crops. The direct and indirect damage caused by various R. solanacearum strains result in reduced yields and quality of crop produce, high costs of production and therefore loss of income, and this is a threat to food and nutritional security. Understanding the R. solanacearum virulence dynamics is essential for effective management of bacterial wilt. Nitric oxide (NO) is known as a key mediator of plant defense responses and functions as a signalling molecule against microbial pathogens. In this study, R. solanacearum, the causal agent of bacterial wilt disease in tomato, was shown to produce NO, which emanates via its denitrification pathway. The effects of NO on the host’s defense response during tomato-R. solanacearum interactions was also investigated and bursts of NO at 6 and 14 h was observed in the tomato root tips of plants inoculated with wild-type R. solanacearum. However, high accumulation of NO was observed in bacterial deletion mutants ΔnorB and ΔhmpX mutants, while very little NO was detected with ∆aniA mutant. R. solanacearum produces much of NO which likely affects the host’s defense response as shown also by eliminating NO from plants via inhibition of NO synthase in aniA mutant. NO-deficient ∆aniA mutant triggered lower expression of the tomato ethylene pathway defense gene PR1 and ACO5, while the NO-accumulating ∆norB and ∆hmpX mutants triggered significantly higher expression. These results show that much NO is produced both by the plant and the pathogen during interactions and further suggests that the pathogen-produced NO plays a significant role in the induction of plant defenses. These insights could potentially be harnessed to come up with effective management systems for this devastating soil borne pathogen.
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RUFORUM Working document series
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