scholarly journals Modifications in Tissue and Cell Ultrastructure as Elements of Immunity-Like Reaction in Chenopodium quinoa against Prune Dwarf Virus (PDV)

Cells ◽  
2020 ◽  
Vol 9 (1) ◽  
pp. 148 ◽  
Author(s):  
Edmund Kozieł ◽  
Katarzyna Otulak-Kozieł ◽  
Józef J. Bujarski
Keyword(s):  
Vascular Tissue ◽  
Chenopodium Quinoa ◽  
Cell Ultrastructure ◽  
Host Cells ◽  
Dwarf Virus ◽  
Ultrastructural Changes ◽  
Viral Pathogen ◽  
Prune Dwarf Virus ◽  
Systemic Spread ◽  
Specific Reactions

Prune dwarf virus (PDV) is a plant RNA viral pathogen in many orchard trees worldwide. Our knowledge about resistance genes or resistant reactions of plant hosts to PDV is scant. To fill in part of this gap, an aim of this study was to investigate reactions to PDV infection in a model host, Chenopodium quinoa. Our investigations concentrated on morphological and ultrastructural changes after inoculation with PDV strain 0599. It turned out that PDV infection can cause deformations in host cells but also induce changes in the organelles, such as chloroplasts in inoculated leaves. Moreover, we also demonstrated specific reactions/changes, which could be associated with both types of vascular tissue capable of effectively blocking the systemic spread of PDV to upper leaves. Furthermore, the relative amount of virus, P1 protein deposition, and movement protein (MP) gene expression consequently decreased in PDV-inoculated leaves.

scholarly journals Ultrastructural Analysis of Prune Dwarf Virus Intercellular Transport and Pathogenesis

2018 ◽  
Vol 19 (9) ◽  
pp. 2570 ◽  
Author(s):  
Edmund Kozieł ◽  
Katarzyna Otulak-Kozieł ◽  
Józef Bujarski
Keyword(s):  
Structural Changes ◽  
Alfalfa Mosaic Virus ◽  
Ultrastructural Level ◽  
Dwarf Virus ◽  
Intercellular Transport ◽  
Viral Pathogen ◽  
Prune Dwarf Virus ◽  
Viral Particles ◽  
Relationship Of

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.

scholarly journals Effective decellularisation of human saphenous veins for biocompatible arterial tissue engineering applications: Bench optimisation and feasibility in vivo testing

2021 ◽  
Vol 12 ◽  
pp. 204173142098752
Author(s):  
Nadiah S Sulaiman ◽  
Andrew R Bond ◽  
Vito D Bruno ◽  
John Joseph ◽  
Jason L Johnson ◽  
...  
Keyword(s):  
Tissue Engineering ◽  
Mechanical Strength ◽  
Vascular Tissue ◽  
Sodium Dodecyl ◽  
Host Cells ◽  
Replacement Model ◽  
In Vivo Testing ◽  
Vascular Scaffolds

Human saphenous vein (hSV) and synthetic grafts are commonly used conduits in vascular grafting, despite high failure rates. Decellularising hSVs (D-hSVs) to produce vascular scaffolds might be an effective alternative. We assessed the effectiveness of a detergent-based method using 0% to 1% sodium dodecyl sulphate (SDS) to decellularise hSV. Decellularisation effectiveness was measured in vitro by nuclear counting, DNA content, residual cell viability, extracellular matrix integrity and mechanical strength. Cytotoxicity was assessed on human and porcine cells. The most effective SDS concentration was used to prepare D-hSV grafts that underwent preliminary in vivo testing using a porcine carotid artery replacement model. Effective decellularisation was achieved with 0.01% SDS, and D-hSVs were biocompatible after seeding. In vivo xeno-transplantation confirmed excellent mechanical strength and biocompatibility with recruitment of host cells without mechanical failure, and a 50% patency rate at 4-weeks. We have developed a simple biocompatible methodology to effectively decellularise hSVs. This could enhance vascular tissue engineering toward future clinical applications.

scholarly journals Loss of a conserved MAPK causes catastrophic failure in assembly of a specialized cilium-like structure in Toxoplasma gondii

2020 ◽  
Vol 31 (9) ◽  
pp. 881-888 ◽  
Author(s):  
William J. O’Shaughnessy ◽  
Xiaoyu Hu ◽  
Tsebaot Beraki ◽  
Matthew McDougal ◽  
Michael L. Reese
Keyword(s):  
Toxoplasma Gondii ◽  
Host Cells ◽  
Ultrastructural Changes ◽  
Catastrophic Failure ◽  
Replicative Cycle

Toxoplasma gondii that lacks the kinase ERK7 cannot invade or egress from their host cells, thereby blocking their replicative cycle. These defects are due to the loss of a specialized cilium-like structure called the conoid. Strikingly, the ultrastructural changes are specific to the conoid, and suggest an important role for ERK7 in its biogenesis.

Comparison of ELISA and RT-PCR for the detection of Prunus necrotic ring spot virus and prune dwarf virus in almond (Prunus dulcis)

2003 ◽  
Vol 114 (1) ◽  
pp. 65-69 ◽  
Author(s):  
Genet Mekuria ◽  
Sunita A. Ramesh ◽  
Evita Alberts ◽  
Terry Bertozzi ◽  
Michelle Wirthensohn ◽  
...  
Keyword(s):  
Prunus Dulcis ◽  
Dwarf Virus ◽  
Rt Pcr ◽  
Spot Virus ◽  
Prune Dwarf Virus ◽  
Ring Spot

scholarly journals The Incidence and Genetic Diversity of Apple Mosaic Virus (ApMV) and Prune Dwarf Virus (PDV) in Prunus Species in Australia

Viruses ◽  
2018 ◽  
Vol 10 (3) ◽  
pp. 136 ◽  
Author(s):  
Wycliff Kinoti ◽  
Fiona Constable ◽  
Narelle Nancarrow ◽  
Kim Plummer ◽  
Brendan Rodoni
Keyword(s):  
Genetic Diversity ◽  
Mosaic Virus ◽  
Dwarf Virus ◽  
Prunus Species ◽  
Prune Dwarf Virus

scholarly journals Salmonella enterica subspecies enterica serovar Enteritidis Salmonella pathogenicity island 2 type III secretion system: role in intestinal colonization of chickens and systemic spread

Microbiology ◽  
2010 ◽  
Vol 156 (9) ◽  
pp. 2770-2781 ◽  
Author(s):  
Amanda L. S. Wisner ◽  
Taseen S. Desin ◽  
Birgit Koch ◽  
Po-King S. Lam ◽  
Emil M. Berberov ◽  
...  
Keyword(s):  
Type Iii Secretion ◽  
Salmonella Enterica ◽  
Type Strain ◽  
Wild Type Strain ◽  
Type Iii Secretion System ◽  
Secretion System ◽  
Host Cells ◽  
Wild Type ◽  
Type Iii ◽  
Systemic Spread

Salmonella enterica subspecies enterica serovar Enteritidis (S. Enteritidis) has been identified as a significant cause of salmonellosis in humans. Salmonella pathogenicity islands 1 and 2 (SPI-1 and SPI-2) each encode a specialized type III secretion system (T3SS) that enables Salmonella to manipulate host cells at various stages of the invasion/infection process. For the purposes of our studies we used a chicken isolate of S. Enteritidis (Sal18). In one study, we orally co-challenged 35-day-old specific pathogen-free (SPF) chickens with two bacterial strains per group. The control group received two versions of the wild-type strain Sal18: Sal18 attTn7 : : tet and Sal18 attTn7 : : cat, while the other two groups received the wild-type strain (Sal18 attTn7 : : tet) and one of two mutant strains. From this study, we concluded that S. Enteritidis strains deficient in the SPI-1 and SPI-2 systems were outcompeted by the wild-type strain. In a second study, groups of SPF chickens were challenged at 1 week of age with four different strains: the wild-type strain, and three other strains lacking either one or both of the SPI-1 and SPI-2 regions. On days 1 and 2 post-challenge, we observed a reduced systemic spread of the SPI-2 mutants, but by day 3, the systemic distribution levels of the mutants matched that of the wild-type strain. Based on these two studies, we conclude that the S. Enteritidis SPI-2 T3SS facilitates invasion and systemic spread in chickens, although alternative mechanisms for these processes appear to exist.

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