Abstract

Sheath blight disease of rice caused by a soil-borne fungal pathogen Rhizoctonia solani AG1-IA is one of the major threats to rice production globally. During host-pathogen interactions, reactive oxygen species (ROS) play an important role in pathogen virulence and plant defense. For example, necrotrophic pathogens induce ROS production to damage host cells, whereas the host can incite ROS to kill the pathogen. From the host perspective, it is essential to understand how the antioxidant machinery maintains a delicate balance of ROS to protect itself from its lethal effects. Here, we investigated the pathogen-induced accumulation of ROS and implicated damage in two rice genotypes (PR114, susceptible; ShB, moderately tolerant) varying in the level of susceptibility to R. solani AG1-IA. Compared to PR114, ShB exhibited a better antioxidant response and reasonably lesser oxidative damage. Further, we observed elevated levels of jasmonic acid (JA) in ShB, which was otherwise decreased in PR114 in response to pathogen infection. As depicted, an elevated level of JA was in agreement with the expression profiles of genes involved in its biosynthesis and signaling. To further ascertain if the heightened antioxidant response is JA-dependent or independent, methyl jasmonate (MeJA) was exogenously applied to PR114, and antioxidant response in terms of gene expression, enzyme activities, and oxidative damage was studied in R. solani infected samples. Surprisingly, the exogenous application of MeJA complemented the antioxidant response and reduced oxidative damage in PR114, thus suggesting that the antioxidant defense system is under transcriptional control of JA.

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