Please use this identifier to cite or link to this item: http://223.31.159.10:8080/jspui/handle/123456789/792
Title: Molecular dissection of extracellular matrix proteome reveals discrete mechanism regulating Verticillium dahliae triggered vascular wilt disease in potato
Authors: Elagamey, Eman
Sinha, Arunima
Narula, Kanika
Abdellatef, Magdi A.E.
Chakraborty, Niranjan
Chakraborty, Subhra
Keywords: Comparative proteomics
Extracellular matrix
Patho-stress
Potato
Vascular wilt
Verticillium dahliae
Issue Date: 2017
Publisher: John Wiley & Sons
Citation: Proteomics, 17(23-24): 1600373
Abstract: 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.
Description: Accepted date: 1 September 2017
URI: http://223.31.159.10:8080/jspui/handle/123456789/792
ISSN: 1615-9861
Appears in Collections:Institutional Publications

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