ANNOUNCEMENTS
Chickpea (Cicer arietinum L.) is a widely cultivated crop which is highly susceptible to Ascochyta Blight (AB) disease. It is caused by Ascochyta rabiei which is a necrotrophic fungal phytopathogen. The Windborne ascospores or seed borne inoculum from A. rabiei infect crop plants and symptoms are visible as small, pale spots on aerial parts which enlarge into elongated lesions during wet, cool weather. To subvert fungal invasion and restrict pathogen growth, host plant deploys a multi-layered immune response at the site of infection. As an initial response, it triggers an oxidative burst in the infected tissue leading to localized host cell death. Necrotrophic pathogens utilize a variety of enzymatic and non-enzymatic antioxidant system or ROS scavenging machinery to evade these responses but underlying mechanisms are largely unknown. Singh et al. (2012) identified 128 unigenes that are highly up regulated in A. rabiei during oxidative stress. In present study, two of these genes, OSR1 and OSR2 were selected for further characterization. With the objective to understand their role in fungal survival, development and virulence, knockout constructs were prepared for these two genes. Using these constructs knockouts of these genes could be generated. To validate the interaction between OSR1 and Actin, OSR1 was fused with N-terminal Venus and actin was fused with C-terminal Venus and BiFC experiment was performed. The BiFC results need to be further investigated in order to find the role of this interaction in fungus. Many actin interacting proteins are known which either polymerize or depolymerize actin filaments and thereby maintain actin dynamics during hyphal tip growth and other developmental processes of fungal pathogens. We hypothesize that absence of OSR1 and OSR2 might impede the oxidative stress responses in fungus leading to decreased pathogenicity.
Key words: Host-pathogen interactions, Oxidative stress, Ascochyta Blight disease.
