Exploring the Role of Plant Growth-Promoting Rhizobacteria in Mitigating Plant Virus Infections

Abstract

Plant viruses are important pathogens accounting for nearly half of emerging plant disease epidemics worldwide. Cucumber mosaic virus and Potato virus Y rank among the top ten viruses in terms of global economic and biological impact. Conventional management strategies, including resistant cultivars, vector control, and cultural practices, often provide limited and environmentally unsustainable protection. An emerging alternative approach involves the use of plant growth-promoting rhizobacteria, which can enhance plant immunity through induced systemic resistance, a defense mechanism primarily regulated by jasmonic acid and ethylene signaling rather than salicylic acid-dependent systemic acquired resistance. This thesis investigated the antiviral potential and the molecular basis of defense priming through SA and JA pathways of three PGPR strains: Pseudomonas fluorescens 89B-27, Serratia marcescens 90-166, and Bacillus subtilis IN937b, against CMV and PVY infections in two model plants, Nicotiana benthamiana and Arabidopsis thaliana. In growth chamber experiments, PGPR suspensions were applied via soil drenching one week before viral inoculation. Viral accumulation in inoculated and systemic leaves was quantified using RT-qPCR, while the expression of key defense-related genes representing salicylic acid, jasmonic acid, and ethylene pathways was analyzed to assess defense priming. Results revealed strain, time, and host-specific variation in PGPR-mediated antiviral protection. In N. benthamiana, P. fluorescens and S. marcescens significantly reduced CMV and PVY titers at all time points (P<0.05), while B. subtilis was not consistent in virus mitigation. In A. thaliana, only P. fluorescens consistently suppressed CMV (P<0.05), and none of the strains reduced PVY accumulation across all time points. To elucidate the molecular mechanisms underlying PGPR-mediated protection against CMV, defense-related genes representing the SA and JA/ET pathways were analyzed using the 2-ΔΔCt method. Gene expression analysis revealed that PGPR alone did not activate defense genes constitutively, but rather established a primed state, as indicated by the transient and pathogen-dependent induction of SA- and JA/ET-responsive markers following CMV infection. P. fluorescens triggered a JA/ET-centered ISR that correlated with reduced viral load, highlighting the importance of pathway-specific priming in antiviral protection. Collectively, these findings advance our understanding of how beneficial rhizobacteria modulate host signaling networks during virus infection and demonstrate the potential of using ISR-based biocontrol strategies for sustainable management of plant viral diseases.