Browsing by Author "Tyagi, Kriti"

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Enzymatic and non-enzymatic functional attributes of plant microbiome
(Elsevier B.V., 2021) Das, Joyati; Yadav, Sunil Kumar; Ghosh, Srayan; Tyagi, Kriti; Magotra, Ankita; Krishnan, Aiswarya; Jha, Gopaljee
Microbiome plays an important role in plant growth and adaptation to various environmental conditions. The cross-talk between host plant and microbes (including microbe-microbe interactions) plays a crucial role in shaping the microbiome. Recent studies have highlighted that plant microbiome is enriched in genes encoding enzymes and natural products. Several novel antimicrobial compounds, bioactive natural products and lytic/degrading enzymes with industrial implications are being identified from the microbiome. Moreover, advancements in metagenomics and culture techniques are facilitating the development of synthetic microbial communities to promote sustainable agriculture. We discuss the recent advancements, opportunities and challenges in harnessing the full potential of plant microbiome.
Evolution of pathogenicity-associated genes in Rhizoctonia solani AG1-IA by genome duplication and transposon-mediated gene function alterations
(BioMed Central Ltd, 2023) Francis, Aleena; Ghosh, Srayan; Tyagi, Kriti; Prakasam, V.; Rani, Mamta; Singh, Nagendra Pratap; Pradhan, Amrita; Sundaram, R. M.; Priyanka, C.; Laha, G. S.; Kannan, C.; Prasad, M. S.; Chattopadhyay, Debasis; Jha, Gopaljee
Background: Rhizoctonia solani is a polyphagous fungal pathogen that causes diseases in crops. The fungal strains are classified into anastomosis groups (AGs); however, genomic complexity, diversification into the AGs and the evolution of pathogenicity-associated genes remain poorly understood. Results: We report a recent whole-genome duplication and sequential segmental duplications in AG1-IA strains of R. solani. Transposable element (TE) clusters have caused loss of synteny in the duplicated blocks and introduced differential structural alterations in the functional domains of several pathogenicity-associated paralogous gene pairs. We demonstrate that the TE-mediated structural variations in a glycosyl hydrolase domain and a GMC oxidoreductase domain in two paralogous pairs affect the pathogenicity of R. solani. Furthermore, to investigate the association of TEs with the natural selection and evolution of pathogenicity, we sequenced the genomes of forty-two rice field isolates of R. solani AG1-IA. The genomic regions with high population mutation rates and with the lowest nucleotide diversity are enriched with TEs. Genetic diversity analysis predicted the genes that are most likely under diversifying and purifying selections. We present evidence that a smaller variant of a glucosamine phosphate N-acetyltransferase (GNAT) protein, predicted to be under purifying selection, and an LPMP_AA9 domain-containing protein, predicted to be under diversifying selection, are important for the successful pathogenesis of R. solani in rice as well as tomato. Conclusions: Our study has unravelled whole-genome duplication, TE-mediated neofunctionalization of genes and evolution of pathogenicity traits in R. solani AG1-IA. The pathogenicity-associated genes identified during the study can serve as novel targets for disease control.
Genome analysis provides insight about pathogenesis of Indian strains of Rhizoctonia solani in rice
(Springer Nature Publishing AG, 2019) Ghosh, Srayan; Mirza, Neelofar; Kanwar, Poonam; Tyagi, Kriti; Jha, Gopaljee
The Rhizoctonia solani species complex is comprised of strains belonging to different anastomosis groups and causes diseases in several economically important crops, including rice. However, individuals within same anastomosis group exhibit distinct morphological and pathological differences on the same host. In this study, we have sequenced the genome of two aggressive Indian strains (BRS11 and BRS13) belonging to AG1-IA anastomosis group and compared them with the available genome of R. solani AG1-IA. We identified several SNPs and Indels in both of these genomes, in comparison to the AG1-IA genome. Furthermore, we observed expansion and emergence of orthogroups in these Indian strains and identified those potentially associated with pathogenesis. Amongst them, transposable elements, cell wall degrading enzymes, transcription factors, and oxalate decarboxylase were noteworthy. The current study unravels genetic variations and identifies genes that might account for pathogenicity variations amongst R. solani strains.
Host alternative NADH:ubiquinone oxidoreductase serves as susceptibility factor to promote pathogenesis of Rhizoctonia solani in plants
(American Phytopathological Society, 2019) Kant, Ravi; Tyagi, Kriti; Ghosh, Srayan; Jha, Gopaljee
Phytopathogens have evolved mechanisms to utilize host genes (commonly known as susceptibility factors) to promote its pathogenesis. Rhizoctonia solani is one of the highly destructive fungal pathogens of various plants, including rice. Previously we had reported differentially regulated rice genes during pathogenesis of R. solani. In this study, we analyzed the role of tomato homologs of two of the rice genes i.e Isoflavone reductase (IFR) and alternative NADH:ubiquinone oxidoreductase (NUOR) as potential susceptibility factors for R. solani. Virus induced gene silencing (VIGS) of NUOR gene in tomato resulted in compromised susceptibility against R. solani, while IFR-silenced plants demonstrated susceptibility similar to that of control plants. NUOR silencing in tomato led to homogenous accumulation of reactive oxygen species (ROS) (optimum range) upon R. solani infection. In addition, expression and enzyme activities of some of the host defense and anti-oxidant genes were enhanced, while H2O2 content, lipid peroxidation and electrolyte leakage were reduced in NUOR-silenced plants. Similarly, transient silencing of OsNUOR gene provided tolerance against R. solani infection in rice. Overall, the data presented in this study suggests that NUOR serves as a host susceptibility factor to promote pathogenesis of R. solani.
The host and pathogen myo-inositol-1-phosphate synthases are required for Rhizoctonia solani AG1-IA infection in tomato
(John Wiley & Sons, 2024) Tyagi, Kriti; Chandan, Ravindra K.; Sahoo, Debashis; Ghosh, Srayan; Gupta, Santosh Kumar; Jha, Gopaljee
The myo-inositol-1-phosphate synthase (MIPS) catalyses the biosynthesis of myo-inositol, an important sugar that regulates various physiological and biochemical processes in plants. Here, we provide evidence that host (SlMIPS1) and pathogen (Rs_MIPS) myo-inositol-1-phosphate synthase (MIPS) genes are required for successful infection of Rhizoctonia solani, a devastating necrotrophic fungal pathogen, in tomato. Silencing of either SlMIPS1 or Rs_MIPS prevented disease, whereas an exogenous spray of myo-inositol enhanced disease severity. SlMIPS1 was upregulated upon R. solani infection, and potentially promoted source-to-sink transition, induced SWEET gene expression, and facilitated sugar availability in the infected tissues. In addition, salicylic acid (SA)-jasmonic acid homeostasis was altered and SA-mediated defence was suppressed; therefore, disease was promoted. On the other hand, silencing of SlMIPS1 limited sugar availability and induced SA-mediated defence to prevent R. solani infection. Virus-induced gene silencing of NPR1, a key gene in SA signalling, rendered SlMIPS1-silenced tomato lines susceptible to infection. These analyses suggest that induction of SA-mediated defence imparts disease tolerance in SlMIPS1-silenced tomato lines. In addition, we present evidence that SlMIPS1 and SA negatively regulate each other to modulate the defence response. SA treatment reduced SlMIPS1 expression and myo-inositol content in tomato, whereas myo-inositol treatment prevented SA-mediated defence. We emphasize that downregulation of host/pathogen MIPS can be an important strategy for controlling diseases caused by R. solani in agriculturally important crops.
Methionine biosynthetic genes and methionine sulfoxide reductase A are required for Rhizoctonia solani AG1-IA to cause sheath blight disease in rice
(John Wiley & Sons, 2024) Das, Joyati; Ghosh, Srayan; Tyagi, Kriti; Sahoo, Debashis; Jha, Gopaljee
Rhizoctonia solani is a polyphagous necrotrophic fungal pathogen that causes sheath blight disease in rice. It deploys effector molecules as well as carbohydrate-active enzymes and enhances the production of reactive oxygen species for killing host tissues. Understanding R. solani ability to sustain growth under an oxidative-stress-enriched environment is important for developing disease control strategies. Here, we demonstrate that R. solani upregulates methionine biosynthetic genes, including Rs_MET13 during infection in rice, and double-stranded RNA-mediated silencing of these genes impairs the pathogen's ability to cause disease. Exogenous treatment with methionine restores the disease-causing ability of Rs_MET13-silenced R. solani and facilitates its growth on 10 mM H2O2-containing minimal-media. Notably, the Rs_MsrA gene that encodes methionine sulfoxide reductase A, an antioxidant enzyme involved in the repair of oxidative damage of methionine, is upregulated upon H2O2 treatment and also during infection in rice. Rs_MsrA-silenced R. solani is unable to cause disease, suggesting that it is important for the repair of oxidative damage in methionine during host colonization. We propose that spray-induced gene silencing of Rs_MsrA and designing of antagonistic molecules that block MsrA activity can be exploited as a drug target for effective control of sheath blight disease in rice.