Abstract

The cell wall provides the structure of the plant, and also acts as a barier against biotic stress. The vein necrosis strain of Potato virus Y (PVYNTN) induces necrotic disease symptoms that affect both plant growth and yield. Virus infection triggers a number of inducible basal defense responses, including defense proteins, especially those involved in cell wall metabolism. This study investigates the comparison of cell wall host dynamics induced in a compatible (potato cv. Irys) and incompatible (potato cv. Sárpo Mira with hypersensitive reaction gene Ny-Smira) PVYNTN–host–plant interaction. Ultrastructural analyses revealed numerous cell wall changes induced by virus infection. Furthermore, the localization of essential defensive wall-associated proteins in susceptible and resistant potato host to PVYNTN infection were investigated. The data revealed a higher level of detection of pathogenesis-related protein 2 (PR-2) in a compatible compared to an incompatible (HR) interaction. Immunofluorescence analyses indicated that hydroxyproline-rich glycoproteins (HRGP) (extensin) synthesis was induced, whereas that of cellulose synthase catalytic subunits (CesA4) decreased as a result of PVYNTN infection. The highest level of extensin localization was found in HR potato plants. Proteins involved in cell wall metabolism play a crucial role in the interaction because they affect the spread of the virus. Analysis of CesA4, PR-2 and HRGP deposition within the apoplast and symplast confirmed the active trafficking of these proteins as a step-in potato cell wall remodeling in response to PVYNTN infection. Therefore, cell wall reorganization may be regarded as an element of “signWALLing”—involving apoplast and symplast activation as a specific response to viruses.

Highlights

  • The cell wall serves both to define and maintain the structural integrity of the plant as well as to protect from external stress

  • The findings reveal changes in the regulation of protein production involved in potato cell wall synthesis (e.g., cellulose synthase subunit 4 (CesA4)), and localization of proteins arranged in cell wall remodeling processes (pathogenesis related protein (PR-2) and hydroxyproline-rich glycoproteins (HRGP))

  • The ultrastructural analyses and precise localization and distribution of cell wall proteins/enzymes permitted the collection in situ of new information on structural changes, reorganization and remodeling within the apoplast and symplast associated with plant-host defense response to virus infection

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Summary

Introduction

The cell wall serves both to define and maintain the structural integrity of the plant as well as to protect from external stress. It functions to adapt the plant to changes during growth and development [1] This involves modifications in composition and structure of the cell wall through sensing and signaling, intercellular communication as well as exchange interfaces [2,3]. The symptoms of PVY infection depend on virus strain and host resistance level. Host response to virus infection is categorized as either compatible (susceptible) or incompatible (resistant) interactions. In the former, the virus spreads systemically throughout the host, whereas in the latter, systemic spread is prevented by localized cell death (hypersensitive response, HR) [6,7]

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