Institutional Publications

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    OsWAKL21, a putative receptor of rice cell wall damage activates alternate signaling in rice and Arabidopsis to induce immunity
    (American Phytopathological Society, 2019) Malukani, K. K.; Ranjan, A.; Hota, S. J.; Patel, H. K.; Sonti, Ramesh V.
    Xanthomonas oryzae pv. oryzae (Xoo) causes the serious bacterial blight disease of rice. As part of its virulence repertoire, Xoo secretes various cell wall degrading enzymes (CWDEs) such as cellulases, xylanases and a Lipase/esterase (LipA). Conversely, treatment of rice tissues with any of these purified enzymes activates immune responses. Plants sense this cell wall damage as a mark of infection and induce immune responses. Very little information is available about the plant functions that are involved in the elaboration of cell wall damage induced immune responses. Transcriptome analyses revealed a rice cell wall-associated receptor kinase, OsWAKL21 that is upregulated following treatment with either LipA or Xoo. VIGS mediated downregulation of OsWAKL21 attenuates LipA induced immune responses. Overexpression of OsWAKL21 in rice mimics LipA treatment in induction of immune responses, activation of JA pathway and enhanced expression of defence related genes, indicating that it plays an important role in elaboration of LipA induced immune responses. Ectopic expression of OsWAKL21 in Arabidopsis also activates plant immune responses. OsWAKL21 is a moonlighting kinase having in vitro kinase and guanylate cyclase activities. Interestingly, OsWAKL21 needs kinase activity to activate immune responses in rice while in Arabidopsis it needs the guanylate cyclase activity. Thus OsWAKL21 is activating similar immune responses in two different species but via different mechanisms.
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    Phase variation in rice pathogen Xanthomonas oryzae pv. oryzae
    (American Phytopathological Society, 2019) Madhavan, V. N.; Patel, H. K.; Patil, P. B.; Sonti, Ramesh V.
    Xanthomonas oryzae pv. oryzae (Xoo) is the causal pathogen of bacterial blight of rice. Diverse factors contribute to its virulence, e.g., secreted enzymes, protein involved in adhesion, gene regulation. Two such studied virulence factors are Exopolysaccharide (EPS) and Lipopolysaccharide (LPS). LPS is a structural component of the outer membrane of all gram-negative bacteria. LPS is necessary for the function of many outer membrane proteins and protect the bacteria from antimicrobial plant products. EPS is a complex polymer secreted by Xanthomonas genus and the known functions of EPS include biofilm formation, and suppression of the plant immune responses. In this study, we isolated non-mucoid and virulence compromised Xoo colonies from stationary phase cultures. These spontaneous mutants are called as stationary phase variants (SPV). Our data show that, SPVs arises due to insertion of endogenous Insertion Sequence (IS) elements in EPS or LPS O-antigen biosynthetic clusters or by slipped-strand mispairing (SSM) in wxoA gene of LPS O-antigen biosynthetic cluster. The SPVs reverts to wild-type colony morphology and showed true reversion, i.e. restoration of wild-type genotype. The results suggest that we are observing phase variation in Xoo. We hypothesize that similar phase variation may be a part of Xoo’s life cycle. Which may help the bacteria survive in nutrient limited conditions during late stages of infection and on rice seeds and plant debris.
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    Immune response induction in rice due to co-expression of XopQ and XopX
    (American Phytopathological Society, 2019) Deb, S.; Patel, H. K.; Sonti, Ramesh V.
    Xanthomonas oryzae pv. oryzae (Xoo) causes bacterial blight, a serious disease of rice. Xoo uses the type III secretion system (T3SS) to suppress rice immune responses. The T3SS secreted effectors XopQ and XopX suppress rice immune responses by interaction with different rice 14-3-3 proteins. Sub-cellular localisation of XopQ and XopX mutants that are defective in 14-3-3 binding and suppression of immune responses indicates that, for suppression, XopQ requires a cytoplasmic localisation whereas XopX requires nuclear localisation. Hence, both XopQ as well as XopX individually act as suppressors of rice immune responses, probably by targeting unique pathways in different subcellular compartments. However, we find that when XopQ is delivered through Agrobacterium along with XopX, it becomes an inducer of immune responses and that it now localizes in the nucleus. We also find that XopQ and XopX can interact with each other. This raises the possibility that besides being a suppressor of immune responses, XopQ can under certain circumstances also function as an inducer of immune responses.
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    Understanding the molecular intricacies of rice-Rhizoctonia solani interactions
    (American Phytopathological Society, 2019) Ghosh, S.; Kanwar, P.; Jha, Gopaljee
    Sheath blight disease is a devastating disease in rice that causes huge crop losses worldwide. It is caused by a necrotrophic fungus Rhizoctonia solani. In spite of global efforts till now there are no reports of complete resistance against this pathogen. We observed that R. solani has a brief biotrophic phase wherein mycelial grows parallel to rice veins without showing any morphological and anatomical changes. However, at later stage, i.e. necrotrophic phase, infection cushions along with anatomical changes are observed at the site of disease symptoms. Through transcriptome and metabolome studies we have identified several candidate host susceptibility factors and pathogenicity determinants that might play an important role during pathogenesis of R. solani in rice. Furthermore, using whole genome studies, we have identified several gene/gene families that might contribute to the aggressiveness of the R. solani strains. Although gene manipulation studies in R. solani is difficult we have devised ways wherein we can functionally characterize these pathogenicity determinants. Overall the present study will help in better understanding of the rice-R. solani pathosystem which would eventually be helpful in developing strategies for durable sheath blight disease tolerance in rice.