Abstract
Characterizing the molecular mechanism involved in nonhost disease resistance is important to understand the adaptations of plant-pathogen interactions. In this study, virus-induced gene silencing (VIGS)-based forward genetics screen was utilized to identify genes involved in nonhost resistance in Nicotiana benthamiana. Genes encoding ribosomal proteins, RPL12 and RPL19, were identified in the screening. These genes when silenced in N. benthamiana caused a delay in nonhost bacteria induced hypersensitive response (HR) with concurrent increase in nonhost bacterial multiplication. Arabidopsis mutants of AtRPL12 and AtRPL19 also compromised nonhost resistance. The studies on NbRPL12 and NbRPL19 double silenced plants suggested that both RPL12 and RPL19 act in the same pathway to confer nonhost resistance. Our work suggests a role for RPL12 and RPL19 in nonhost disease resistance in N. benthamiana and Arabidopsis. In addition, we show that these genes also play a minor role in basal resistance against virulent pathogens.
Highlights
Disease resistance mechanisms of plants are continuously evolving for the sole purpose of negating the attempted infections of the ever adapting pathogens
To identify plant genes involved in nonhost disease resistance, clones from a normalized N. benthamiana cDNA library (Anand et al, 2007; Senthil-Kumar et al, 2013) were individually silenced using Tobacco rattle virus (TRV)-based virus-induced gene silencing (VIGS) (Senthil-Kumar and Mysore, 2014) and screened for altered hypersensitive response (HR) to nonhost pathogen infection
The bacterial multiplication in the plants was quantified at 3 and 5 dpi (Figure 3). At both these time points, the bacterial multiplication in NbRPL12 and NbRPL19 silenced plants were 10–100-fold higher as compared to the vector-only control plants (Figure 3). These results suggest that NbRPL12 and NbRPL19 silenced plants were compromised for nonhost resistance even when inoculated by dip inoculation method
Summary
Disease resistance mechanisms of plants are continuously evolving for the sole purpose of negating the attempted infections of the ever adapting pathogens. The well-studied resistance (R)-gene mediated disease resistance is often very specific to a particular plant genotype or cultivar and a particular race of a pathogen. Several aspects of plant disease resistance mechanisms and the adaptation of pathogens to overcome the plant defense have been studied and the resistance pathways have been elucidated (Abramovitch and Martin, 2004; Block et al, 2008). Plants respond to pathogen infection by a weak and generic response called as basal resistance (Senthil-Kumar and Mysore, 2013). This defense response reduces the virulent pathogen growth and may delay the disease development
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