Shift in SAR to ISR during the Rice- R. Solani interaction mediated by Streptomyces hyderabadensis confers sheath blight resistance in susceptible genotype

Abstract

Rice sheath blight disease is caused by the necrotrophic pathogen Rhizoctonia solani Kuhn (teleomorph; Thanatephorus cucumeris). Several studies have reported the disease suppression mechanisms in resistant varieties based on innate and systemic acquired resistance (SAR) mechanisms. The resistant varieties turn susceptible due to the intelligence of pathogen strains to mimic plant defense signaling mechanisms. An alternative and ecofriendly approach to tackle the negative effects of plant-pathogen interaction is the application of bio-control agents. Actinobacteria is known for production of secondary metabolites under stress that initiates pre-signaling to enable induced immunity at early plant stages to tackle the pathogen attack during the later stages of plant development. The current study is focused on understanding of mechanisms that provide resistance to rice plants against R. solani in presence of actinobacteria, Streptomyces hyderabadensis, based on biochemical and mRNA/transcript level analysis. The sheath blight incidence was significantly reduced and the disease score was maintained at 1 (lesion height less than 10%) compared to pathogen control. Biochemical analysis revealed that the actinobacterial inoculation enhanced the levels of phenyl ammonia lyase, phenol, polyphenol oxidases, catalases and peroxidases during the tripartite interaction that provided initial resistance and protection from ROS generated during pathogen infection through detoxification process. During the interaction, higher expression of chitinase gene, improvement in chlorophyll content by the expression of chlorophyll a-b binding protein, maintenance of plant overall development by maintaining the balance of melatonin production, lower expression of SAR supportive genes (PAL, ICS, GST) at the later intervals, expression of signaling proteins (14-3-3 like protein GF14-E) to activate the defense related proteins and the proteins that supports the SAR to ISR shift (NPR1) in presence of S. hyderabadensis under pathogen pressure of R. solani.