scholarly journals Novel System for the Simultaneous Analysis ofGeminivirus DNA Replication and Plant Interactions in Nicotianabenthamiana

2003 ◽  
Vol 77 (24) ◽  
pp. 13315-13322 ◽  
Author(s):  
Yiguo Hong ◽  
John Stanley ◽  
Rene van Wezel
Keyword(s):  
Defense Mechanism ◽  
Intracellular Localization ◽  
Potato Virus X ◽  
African Cassava Mosaic Virus ◽  
Origin Of Replication ◽  
Amino Acid Residues ◽  
Plant Interactions ◽  
In Planta ◽  
Gfp Fusion Protein ◽  
Host Defense Mechanism

ABSTRACT The origin of replication of African cassava mosaic virus (ACMV) and a gene expression vector based on Potato virus X were exploited to devise an in planta system for functional analysis of the geminivirus replication-associated protein (Rep) in transgenic Nicotiana benthamiana line pOri-2. This line contains an integrated copy of a tandem repeat of the ACMV origin of replication flanking nonviral sequences that can be mobilized and replicated by Rep as an episomal replicon. A Rep-GFP fusion protein can also mobilize and amplify the replicon, facilitating Rep detection in planta. The activity of Rep and its mutants, Rep-mediated host response, and the correlation between Rep intracellular localization and biological functions could be effectively assessed by using this in planta system. Our results indicate that modification of amino acid residues R2, R5, R7 and K11 or H56, L57 and H58 prevent Rep function in replication. This defect correlates with possible loss of Rep nuclear localization and inability to trigger the host defense mechanism resembling a hypersensitive response.

scholarly journals Unravelling the Pathogenesis and Molecular Interactions of Liberibacter Phytopathogens with Their Psyllid Vectors

Agronomy ◽  
2020 ◽  
Vol 10 (8) ◽  
pp. 1132
Author(s):  
Poulami Sarkar ◽  
Murad Ghanim
Keyword(s):  
Defense Mechanism ◽  
Insect Host ◽  
Plant Interactions ◽  
Molecular Processes ◽  
Citrus Greening Disease ◽  
Zebra Chip Disease ◽  
Economic Threat ◽  
Host Defense Mechanism ◽  
Candidatus Liberibacter ◽  
Important Milestone

Insect-borne bacterial pathogens pose a global economic threat to many agricultural crops. Candidatus liberibacter species, vectored by psyllids (Hemiptera: psylloidea), are an example of devastating pathogens related to important known diseases such as Huanglongbing or the citrus greening disease, Zebra chip disease, and carrot yellowing, along with vegetative disorders in umbellifers. Studies on liberibacter–plant interactions have gained more focus in disease control over the last few decades. However, successful and sustainable disease management depends on the early disruption of insect–pathogen interactions, thereby blocking transmission. Recent knowledge on the liberibacter genomes and various omics approaches have helped us understand this host–pathogen relationship, despite the complexity associated with the inability to culture these bacteria. Here, we discuss the cellular and molecular processes involved in the response of insect-host immunity, and the liberibacter-associated pathogenesis mechanisms that involve virulence traits and effectors released to manipulate the insect–host defense mechanism for successful transmission. Understanding such mechanisms is an important milestone for developing sustainable means for preventing liberibacter transmission by psyllids.

scholarly journals The IL-33-ILC2 pathway protects from amebic colitis

2021 ◽  
Author(s):  
Md Jashim Uddin ◽  
Jhansi L. Leslie ◽  
Stacey L. Burgess ◽  
Noah Oakland ◽  
Brandon Thompson ◽  
...  
Keyword(s):  
Tissue Damage ◽  
Cell Injury ◽  
Defense Mechanism ◽  
Protozoan Parasite ◽  
Lymphoid Cells ◽  
Amebic Colitis ◽  
Host Defense Mechanism ◽  
Important Host ◽  
Murine Colon

AbstractEntamoeba histolytica is a pathogenic protozoan parasite that causes intestinal colitis, diarrhea, and in some cases, liver abscess. Through transcriptomics analysis, we observed that E. histolytica infection was associated with increased expression of IL-33 mRNA in both the human and murine colon. IL-33, the IL-1 family cytokine, is released after cell injury to alert the immune system of tissue damage. Treatment with recombinant IL-33 protected mice from amebic infection and intestinal tissue damage; moreover, blocking IL-33 signaling made mice more susceptible to amebiasis. IL-33 limited the recruitment of inflammatory immune cells and decreased the pro-inflammatory cytokine IL-6 in the cecum. Type 2 immune responses were upregulated by IL-33 treatment during amebic infection. Interestingly, administration of IL-33 protected RAG2–/– mice but not RAG2−/−γc−/− mice, demonstrating that IL-33-mediated protection required the presence of innate lymphoid cells (ILCs). IL-33 induced recruitment of ILC2 but not ILC1 and ILC3 in RAG2−/− mice. At baseline and after amebic infection, there was a significantly higher IL13+ILC2s in C57BL/J mice, which are naturally resistant to amebiasis, than CBA/J mice. Adoptive transfer of ILC2s to RAG2−/−γc−/− mice restored IL-33-mediated protection. These data reveal that the IL-33-ILC2 pathway is an important host defense mechanism against amebic colitis.

scholarly journals Specific hypersensitive response-associated recognition of new apoplastic effectors fromCladosporium fulvumin wild tomato

2017 ◽  
Author(s):  
Carl H. Mesarich ◽  
Bilal Ökmen ◽  
Hanna Rovenich ◽  
Scott A. Griffiths ◽  
Changchun Wang ◽  
...  
Keyword(s):  
Hypersensitive Response ◽  
Expression System ◽  
Potato Virus X ◽  
Cladosporium Fulvum ◽  
In Planta ◽  
Antimicrobial Proteins ◽  
Wild Tomato ◽  
Microbe Interactions ◽  
Leaf Apoplast ◽  
Tomato Leaf Mould

ABSTRACTTomato leaf mould disease is caused by the biotrophic fungusCladosporium fulvum. During infection,C. fulvumproduces extracellular small secreted protein (SSP) effectors that function to promote colonization of the leaf apoplast. Resistance to the disease is governed byCfimmune receptor genes that encode receptor-like proteins (RLPs). These RLPs recognize specific SSP effectors to initiate a hypersensitive response (HR) that renders the pathogen avirulent.C. fulvumstrains capable of overcoming one or more of all clonedCfgenes have now emerged. To combat these strains, newCfgenes are required. An effectoromics approach was employed to identify wild tomato accessions carrying newCfgenes. Proteomics and transcriptome sequencing were first used to identify 70 apoplasticin planta-inducedC. fulvumSSPs. Based on sequence homology, 61 of these SSPs were novel or lacked known functional domains. Seven, however, had predicted structural homology to antimicrobial proteins, suggesting a possible role in mediating antagonistic microbe−microbe interactionsin planta. Wild tomato accessions were then screened for HR-associated recognition of 41 SSPs using thePotato virus X-based transient expression system. Nine SSPs were recognized by one or more accessions, suggesting that these plants carry newCfgenes available for incorporation into cultivated tomato.

scholarly journals Dram1 confers resistance to Salmonella infection

2021 ◽  
Author(s):  
Samrah Masud ◽  
Rui Zhang ◽  
Tomasz K. Prajsnar ◽  
Annemarie H. Meijer
Keyword(s):  
Defense Mechanism ◽  
Early Response ◽  
Protective Role ◽  
Infection Model ◽  
Transgenic Zebrafish ◽  
Functional Link ◽  
Morpholino Knockdown ◽  
Host Defense Mechanism ◽  
Important Host

Dram1 is a stress and infection inducible autophagy modulator that functions downstream of transcription factors p53 and NFκB. Using a zebrafish embryo infection model, we have previously shown that Dram1 provides protection against the intracellular pathogen Mycobacterium marinum by promoting the p62-dependent xenophagy of bacteria that have escaped into the cytosol. However, the possible interplay between Dram1 and other anti-bacterial autophagic mechanisms remains unknown. Recently, LC3-associated phagocytosis (LAP) has emerged as an important host defense mechanism that requires components of the autophagy machinery and targets bacteria directly in phagosomes. Our previous work established LAP as the main autophagic mechanism by which macrophages restrict growth of Salmonella Typhimurium in a systemically infected zebrafish host. We therefore employed this infection model to investigate the possible role of Dram1 in LAP. Morpholino knockdown or CRISPR/Cas9-mediated mutation of Dram1 led to reduced host survival and increased bacterial burden during S. Typhimurium infections. In contrast, overexpression of dram1 by mRNA injection curtailed Salmonella replication and reduced mortality of the infected host. During the early response to infection, GFP-Lc3 levels in transgenic zebrafish larvae correlated with the dram1 expression level, showing over two-fold reduction of GFP-Lc3-Salmonella association in dram1 knockdown or mutant embryos and an approximately 30% increase by dram1 overexpression. Since LAP is known to require the activity of the phagosomal NADPH oxidase, we used a Salmonella biosensor strain to detect bacterial exposure to reactive oxygen species (ROS) and found that the ROS response was largely abolished in the absence of dram1. Together, these results demonstrate the host protective role of Dram1 during S. Typhimurium infection and suggest a functional link between Dram1 and the induction of LAP.

scholarly journals Human Serum Albumin Is an Essential Component of the Host Defense Mechanism Against Clostridium difficile Intoxication

2018 ◽  
Vol 218 (9) ◽  
pp. 1424-1435 ◽  
Author(s):  
Alessandra di Masi ◽  
Loris Leboffe ◽  
Fabio Polticelli ◽  
Federica Tonon ◽  
Cristina Zennaro ◽  
...  
Keyword(s):  
Clostridium Difficile ◽  
Human Serum Albumin ◽  
Serum Albumin ◽  
Human Serum ◽  
Host Defense ◽  
Defense Mechanism ◽  
Essential Component ◽  
Host Defense Mechanism

scholarly journals Mitofusin 2-Deficiency Suppresses Mycobacterium tuberculosis Survival in Macrophages

Cells ◽  
2019 ◽  
Vol 8 (11) ◽  
pp. 1355 ◽  
Author(s):  
Junghwan Lee ◽  
Ji-Ae Choi ◽  
Soo-Na Cho ◽  
Sang-Hun Son ◽  
Chang-Hwa Song
Keyword(s):  
Mycobacterium Tuberculosis ◽  
Molecular Mechanisms ◽  
Defense Mechanism ◽  
Mitochondrial Fission ◽  
Mycobacterial Infection ◽  
Mitofusin 2 ◽  
Unstimulated Control ◽  
Host Defense Mechanism ◽  
Important Host

Apoptosis is an important host defense mechanism against mycobacterial infection. However, the molecular mechanisms regulating apoptosis during mycobacterial infection are not well known. Recent reports suggest that bacterial infection regulates mitochondrial fusion and fission in various ways. Here, we investigated the role of mitochondria in Mycobacterium tuberculosis (Mtb)-infected macrophages. Mtb H37Rv (Rv) infection induced mitofusin 2 (MFN2) degradation, leading to mitochondrial fission. Interestingly, Mtb H37Ra (Ra) infection induced significantly greater mitochondrial fragmentation than Rv infection. Mtb-mediated Parkin, an E3 ubiquitin ligase, contributed to the degradation of MFN2. To evaluate the role of endoplasmic reticulum stress in the production of Parkin during Mtb infection, we analyzed Parkin production in 4-phenylbutyric acid (4-PBA)-pretreated macrophages. Pretreatment with 4-PBA reduced Parkin production in Mtb-infected macrophages. In contrast, the level of MFN2 production recovered to a level similar to that of the unstimulated control. In addition, Ra-infected macrophages had reduced mitochondrial membrane potential (MMP) compared to those infected with Rv. Interestingly, intracellular survival of mycobacteria was decreased in siMFN2-transfected macrophages; in contrast, overexpression of MFN2 in macrophages increased Mtb growth compared with the control.

scholarly journals Increased CD11b and Decreased CD62L in Blood and Airway Neutrophils from Long-Term Smokers with and without COPD

2020 ◽  
Vol 12 (6) ◽  
pp. 480-489
Author(s):  
Marit Stockfelt ◽  
Karin Christenson ◽  
Anders Andersson ◽  
Lena Björkman ◽  
Médea Padra ◽  
...  
Keyword(s):  
Surface Density ◽  
Defense Mechanism ◽  
Ex Vivo ◽  
Study Groups ◽  
Lower Surface ◽  
Chronic Obstructive ◽  
Obstructive Pulmonary Disease ◽  
Host Defense Mechanism ◽  
Blood Neutrophils

There is incomplete mechanistic understanding of the mobilization of neutrophils in the systemic and local compartment in smokers with chronic obstructive pulmonary disease (COPD). In this pilot study, we characterized how the adhesion molecules CD11b and CD62L, surface markers indicative of priming, are altered as neutrophils extravasate, and whether surface density of CD11b and CD62L differs between long-term tobacco smokers (LTS) with and without COPD compared with healthy never-smokers (HNS). Unstimulated blood neutrophils from LTS with (<i>n</i> = 5) and without (<i>n</i> = 9) COPD displayed lower surface density of CD62L compared with HNS (<i>n</i> = 8). In addition, surface density of CD11b was higher in bronchoalveolar lavage (BAL) neutrophils from LTS without COPD compared with those with COPD and HNS. Moreover, in BAL neutrophils from all study groups, CD62L was lower compared with matched blood neutrophils. In addition, BAL neutrophils responded with a further decrease in CD62L to ex vivo TNF stimulation. Thus, neutrophils in the airway lumen display a higher state of priming than systemic neutrophils and bear the potential to be further primed by local cytokines even with no smoking or the presence of COPD, findings that may represent a universal host defense mechanism against local bacteria. Moreover, systemic neutrophils are primed in LTS regardless of COPD. Further studies in larger materials are warranted to determine whether the priming of neutrophils is protective against COPD or merely preceding it.

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