Publications of NIPGR Scientists

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Chitosan-triggered immunity to Fusarium in chickpea is associated with changes in the plant extracellular matrix architecture, stomatal closure and remodelling of the plant metabolome and proteome
(John Wiley & Sons, 2020) Narula, Kanika; Elagamey, Eman; Abdellatef, Magdi A.E.; Sinha, Arunima; Ghosh, Sudip; Chakraborty, Niranjan; Chakraborty, Subhra
Pathogen/microbe associated molecular patterns (PAMPs/MAMPs) initiate complex defense responses by reorganizing the biomolecular dynamics of the host cellular machinery. The extracellular matrix (ECM) acts as a physical scaffold that prevents recognition and entry of phyto‐pathogens, while guard cells perceive and integrate signals metabolically. Although chitosan is known MAMP implicated in plant defense, the precise mechanism of chitosan‐triggered immunity (CTI) remains unknown. Here, we show how chitosan imparts immunity against fungal disease. Morpho‐histological examination revealed stomatal closure accompanied by reductions in stomatal conductance and transpiration rate as early responses in chitosan‐treated seedlings upon vascular fusariosis. Electron microscopy and Raman spectroscopy showed ECM fortification leading to oligosaccharide signaling, as documented by increased galactose, pectin and associated secondary metabolites. Multiomics approach using quantitative ECM proteomics and metabolomics identified 325 chitosan‐triggered immune‐responsive proteins (CTIRPs) notably novel ECM structural proteins, LYM2 and receptor‐like kinases, and 65 chitosan‐triggered immune‐responsive metabolites (CTIRMs), including sugars, sugar alcohols, fatty alcohols, organic and amino acids. Identified proteins and metabolites are linked to ROS production, stomatal movement, root nodule development and root architecture coupled with oligosaccharide signaling that leads to Fusarium resistance. The cumulative data demonstrate that ROS, NO and eATP govern CTI, in addition to induction of PR proteins, CAZymes and PAL activities, besides accumulation of phenolic compounds downstream of CTI. The immune‐related correlation network identified functional hubs in the CTI pathway. Altogether, these shifts led to the discovery of chitosan‐responsive networks that cause significant ECM and guard cell remodeling and translate ECM cues into cell fate decisions during fusariosis.
Molecular dissection of extracellular matrix proteome reveals discrete mechanism regulating Verticillium dahliae triggered vascular wilt disease in potato
(John Wiley & Sons, 2017) Elagamey, Eman; Sinha, Arunima; Narula, Kanika; Abdellatef, Magdi A.E.; Chakraborty, Niranjan; Chakraborty, Subhra
Plants exposed to patho-stress mostly succumb due to disease by disruption of cellular integrity and changes in the composition of the extracellular matrix (ECM). Vascular wilt, caused by the soil borne hemibiotrophic filamentous fungus Verticillium dahliae, is one of the most significant diseases that adversely affects plant growth and productivity. The virulence of the pathogen associated with the ECM-related susceptibility of the host plant is far from being understood. To better understand ECM-associated disease responses that allow the pathogen to supress plant immunity, a temporal analysis of ECM proteome was carried out in vascular wilt susceptible potato cultivar upon V. dahliae infection. The proteome profiling led to the identification of 75 patho-stress responsive proteins (PSRPs), predominantly involved in wall hydration, architecture, and redox homeostasis. Two novel clues regarding wilt disease of potato were gained from this study. First, wall crosslinking and salicylic acid signaling significantly altered during patho-stress. Second, generation of reactive oxygen species and scavenging proteins increased in abundance leading to cell death and necrosis of the host. We provide evidence for the first time that how fungal invasion affects the integrity of ECM components and host reprogramming for susceptibility may function at the cell surface by protein plasticity. This article is protected by copyright. All rights reserved.
Quantitative extracellular matrix proteomics suggests cell wall reprogramming in host-specific immunity during vascular wilt caused by Fusarium oxysporum in chickpea
(John Wiley & Sons, 2017) Elagamey, Eman; Narula, Kanika; Sinha, Arunima; Ghosh, Sudip; Abdellatef, Magdi A.E.; Chakraborty, Niranjan; Chakraborty, Subhra
Extracellular matrix (ECM) is the unique organelle that perceives stress signals and reprograms molecular events of host cell during patho-stress. However, our understanding of how ECM dictates plant immunity is largely unknown. Vascular wilt caused by the soil borne filamentous fungus Fusarium oxysporum is a major impediment for global crop productivity. To elucidate the role of ECM proteins and molecular mechanism associated with cell wall mediated immunity, the temporal changes of ECM proteome was studied in vascular wilt resistant chickpea cultivar upon F. oxysporum infection. The 2-DE protein profiling coupled with mass spectrometric analysis identified 166 immune responsive proteins (IRPs) involved in variety of functions. Our data suggest that wall remodeling; protein translocation, stabilization and chitin triggered immunity; extracellular ATP signaling are major players in early, middle and later phases of ECM signaling during fungal attack. Furthermore, we interrogated the proteome data using network analysis that identified modules enriched in known and novel immunity-related prognostic proteins centered around nascent aminopolypeptide complex (NAC), amine oxidase, thioredoxin and chaperonin. This study for the first time provides an insight into the complex network operating in the ECM and impinges on the surveillance mechanism of innate immunity during patho-stress in crop plant.