A molecular tug-of-war: Global plant proteome changes during viral infection

Alexander, M.; Cilia, Michelle

doi:10.1016/j.cpb.2015.10.003

Cited by 41 publications

(42 citation statements)

References 142 publications

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“…Plant viruses change the expression of plant genes leading to structural deformations. Plasmodesmata (PD) and the cell wall are amongst the highly modified structures [ 42 , 43 ]. For PDs, the host plant tries to block the path to stop the viral cell-to-cell transport [ 31 ], e.g., via callose depositions [ 44 ].…”

Section: Discussionmentioning

confidence: 99%

Ultrastructural Analysis of Prune Dwarf Virus Intercellular Transport and Pathogenesis

Kozieł

Otulak

Bujarski

2018

IJMS

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Prune dwarf virus (PDV) is an important viral pathogen of plum, sweet cherry, peach, and many herbaceous test plants. Although PDV has been intensively investigated, mainly in the context of phylogenetic relationship of its genes and proteins, many gaps exist in our knowledge about the mechanism of intercellular transport of this virus. The aim of this work was to investigate alterations in cellular organelles and the cell-to-cell transport of PDV in Cucumis sativus cv. Polan at ultrastructural level. To analyze the role of viral proteins in local transport, double-immunogold assays were applied to localize PDV coat protein (CP) and movement protein (MP). We observe structural changes in chloroplasts, mitochondria, and cellular membranes. We prove that PDV is transported as viral particles via MP-generated tubular structures through plasmodesmata. Moreover, the computer-run 3D modeling reveals structural resemblances between MPs of PDV and of Alfalfa mosaic virus (AMV), implying similarities of transport mechanisms for both viruses.

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Section: Discussionmentioning

confidence: 99%

Ultrastructural Analysis of Prune Dwarf Virus Intercellular Transport and Pathogenesis

Kozieł

Otulak

Bujarski

2018

IJMS

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“…In the first interaction the virus potentially replicates and spreads systemically, whereas in the second, the systemic spread is frequently limited by the localised cell death, induced by the HR (hypersensitive response) [4,5]. In some experimental systems the virus might not be completely blocked [6].…”

Section: Introductionmentioning

confidence: 99%

Spatiotemporal Changes in Xylan-1/Xyloglucan and Xyloglucan Xyloglucosyl Transferase (XTH-Xet5) as a Step-In of Ultrastructural Cell Wall Remodelling in Potato–Potato Virus Y (PVYNTN) Hypersensitive and Susceptible Reaction

Otulak

Kozieł

Bujarski

2018

IJMS

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One type of monitoring system in a plant cell is the cell wall, which intensively changes its structure during interaction with pathogen-stress factors. The wall plays a role as a dynamic and controlled structure, although it is not fully understood how relevant these modifications are to the molecular mechanisms during plant–virus interactions. In this work we localise the non-cellulosic polysaccharides such as xyloglucan, xylan (xylan-1) and xyloglucosyl transferase (XTH-Xet5), the enzyme that participates in the metabolism of xyloglucan. This provided us with information about the in situ distribution of the components of the hemicellulotic cell wall matrix in hypersensitive and susceptible potato–PVYNTN interactions. The loosening of the cell wall was accompanied by an increase in xylan depositions during susceptible interactions, whereas, during the hypersensitive response, when the cell wall was reinforced, the xylan content decreased. Moreover, the PVY inoculation significantly redirected XTH-Xet5 depositions, regardless of types of interactions, compared to mock-inoculated tissues. Furthermore, the immunogold localisation clearly revealed the domination of Xet5 in the cell wall and in vesicles in the susceptible host. In contrast, in the resistant host increased levels of Xet5 were observed in cytoplasm, in the cell wall and in the trans-Golgi network. These findings show that the hypersensitive reaction activated XTH-Xet5 in the areas of xyloglucan endo-transglycosylase (XET) synthesis, which was then actively transported to cytoplasm, cell wall and to vacuoles. Our results provide novel insight into cell wall reorganisation during PVYNTN infection as a response to biotic stress factors. These novel findings help us to understand the mechanisms of defence responses that are incorporated into the cell wall signalling network.

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“…Isobaric tag for relative and absolute quantitation LC-MS/MS (liquid chromatography tandem mass spectrometry) technology has been used to study virus-host interactions. Previous tudies have compared virus-infected plants with healthy plants to understand these interactions (Wang et al 2015;Alexander and Cilia 2016;Chen et al 2017). In this study, we compared the proteome profiles of plants infected with TMV and a fasterreplicating mutant TMV 24A + UPD.…”

Section: Discussionmentioning

confidence: 99%

iTRAQ-based quantitative proteomics reveals a ferroptosis-like programmed cell death in plants infected by a highly virulent tobacco mosaic virus mutant 24A+UPD

et al. 2020

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Plants trigger a highly orchestrated defence mechanism in response to viral infection. In this study, we aimed at understanding the molecular events that lead to more accelerated cell death in Nicotiana benthamiana plants infected with the fast-replicating TMV 24A + UPD in comparison to TMV. TMV 24A + UPD is an artificial mutant that induces more severe symptoms leading to precocious death in plants. We employed the iTRAQ-based quantitative proteomics approach to identify and map the proteomes of TMV and TMV 24A + UPD infected plants at time points that correlate with initiation of early cell death symptoms. TMV 24A + UPD proteome profile revealed 183 highly abundant proteins versus 71 for TMV infected plants. KEGG analysis revealed differentially abundant proteins in the two proteome profiles under cell death, stress signalling, protein folding, sorting, degradation, transport and catabolism. We identified unique differentially abundant proteins in the TMV 24A + UPD profile, in particular under the ferroptosis and glutathione metabolism pathways. For validation, we varied the amount of intracellular iron by supplementing plants with Fe 3+ , employing iron chelators and by virus induced gene silencing of iron storage protein ferritin gene. We also employed potent ferroptosis inhibitors ferostatin-1, liprostatin-1, and transiently silenced glutathione peroxidase 4 gene. TMV 24A + UPD infected plants showed accelerated cell death symptoms when intracellular iron was increased. Decreasing intracellular iron protected the plants from accelerated cell death. We also observed a decrease in TMV 24A + UPD induced cell death when we applied ferroptosis inhibitors. Glutathione peroxidase 4 gene-silenced plants showed enhanced cell death compared to non-silenced control plants. Our study uncovered a link between intracellular iron and accelerated lipid ROS-induced cell death in TMV 24A + UPD infected plants. We propose that the fast-replicating mutant of TMV induces a distinct and potent form of cell death akin to ferroptosis.

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A molecular tug-of-war: Global plant proteome changes during viral infection

Cited by 41 publications

References 142 publications

Ultrastructural Analysis of Prune Dwarf Virus Intercellular Transport and Pathogenesis

Ultrastructural Analysis of Prune Dwarf Virus Intercellular Transport and Pathogenesis

Spatiotemporal Changes in Xylan-1/Xyloglucan and Xyloglucan Xyloglucosyl Transferase (XTH-Xet5) as a Step-In of Ultrastructural Cell Wall Remodelling in Potato–Potato Virus Y (PVYNTN) Hypersensitive and Susceptible Reaction

iTRAQ-based quantitative proteomics reveals a ferroptosis-like programmed cell death in plants infected by a highly virulent tobacco mosaic virus mutant 24A+UPD

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