Please use this identifier to cite or link to this item: http://223.31.159.10:8080/jspui/handle/123456789/792
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dc.contributor.authorElagamey, Eman-
dc.contributor.authorSinha, Arunima-
dc.contributor.authorNarula, Kanika-
dc.contributor.authorAbdellatef, Magdi A.E.-
dc.contributor.authorChakraborty, Niranjan-
dc.contributor.authorChakraborty, Subhra-
dc.date.accessioned2017-10-03T07:05:12Z-
dc.date.available2017-10-03T07:05:12Z-
dc.date.issued2017-
dc.identifier.citationProteomics, 17(23-24): 1600373en_US
dc.identifier.issn1615-9861-
dc.identifier.urihttp://223.31.159.10:8080/jspui/handle/123456789/792-
dc.descriptionAccepted date: 1 September 2017en_US
dc.description.abstractPlants 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.en_US
dc.description.sponsorshipThis work was supported by grants from National Institute of Plant Genome Research, New Delhi, India and Department of Biotechnology, Govt. of India (No.BT/HRD/35/01/05/2013) to S.C. E.E. was the recipient of post-doctoral fellowship from DBT-TWAS. M.A. was the recipient of post-doctoral fellowship from DBT-TWAS. K.N. is the recipient of post-doctoral fellowship from Department of Biotechnology (DBT), Govt. of India. A.S. is the recipient of pre-doctoral fellowship from the Council of Scientific and Industrial research (CSIR), Govt. of India. Authors also thank Jasbeer Singh for illustrations and graphical representations in the manuscript.en_US
dc.language.isoen_USen_US
dc.publisherJohn Wiley & Sonsen_US
dc.subjectComparative proteomicsen_US
dc.subjectExtracellular matrixen_US
dc.subjectPatho-stressen_US
dc.subjectPotatoen_US
dc.subjectVascular wilten_US
dc.subjectVerticillium dahliaeen_US
dc.titleMolecular dissection of extracellular matrix proteome reveals discrete mechanism regulating Verticillium dahliae triggered vascular wilt disease in potatoen_US
dc.typeArticleen_US
dc.identifier.officialurlhttp://onlinelibrary.wiley.com/doi/10.1002/pmic.201600373/fullen_US
dc.identifier.doi10.1002/pmic.201600373en_US
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