Arabidopsis thaliana
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA244971 | ENA |
REPOSITORIES: ENA
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Project description:Arabidopsis was transformed with the NIK receptor or the mutant T474D NIK receptor and infected with CaLCuV. The global variation of gene expression was analysed by RNA-seq at 10 days post inoculation and 20 days post inoculation and differential gene expression was determinated in comparison with mock inoculated Arabidopsis lines.
2014-04-21 | GSE56922 | GEO
Project description:Arabidopsis was transformed with the NIK receptor or the mutant T474D NIK receptor and infected with CaLCuV. The global variation of gene expression was analysed by RNA-seq at 10 days post inoculation and 20 days post inoculation and differential gene expression was determinated in comparison with mock inoculated Arabidopsis lines. Pairwise comparison between mock inoculated and infected genotypes (WT,NIK-expressing lines and T474D-expressing lines) at 10 dpi and 20 dpi
2014-04-21 | E-GEOD-56922 | biostudies-arrayexpress
Project description:To generate an efficient defense against begomovirus, we modulated the activity of the immune defense receptor NIK (NSP-Interacting Kinase) in tomato plants; NIK is a virulence target of the begomovirus NSP during infection. Replacing threonine-474 with aspartate (T474D) within the kinase activation loop promoted the constitutive activation of NIK-mediated defenses. This activation resulted in the down-regulation of translation-related genes and the suppression of global translation in T474D-overexpressing tomato lines. We also found that T474D-induced defense-related transcripts were associated with polysomes and immune proteins, which accumulated to detectable levels in T474D leaves. Consistent with these findings, T474D transgenic lines were tolerant to the tomato-infecting begomoviruses ToYSV and ToSRV. We propose that NIK mediates an anti-viral response via translation suppression and immune system induction. Global variation on gene expression induced by NIK expression and virus infection using total RNA from mock-inoculated and ToYSV-infected tomato wild-type plants, mock-inoculated and infected 35S::NIK1-4 overexpressing lines and mock-inoculated and infected 35S::T474D overexpressing lines. File map_itag23.csv correlates the ITAG 2.3 cDNA ID with the 21 bp reads in file Profiles_with_differential_expressions.csv.
2013-12-17 | E-GEOD-38028 | biostudies-arrayexpress
Project description:The NF-κB pathway is a master regulator of inflammatory processes and is implicated in insulin resistance and pancreatic beta cell dysfunction in the metabolic syndrome. While canonical NF-κB signaling is well studied, there is little information on the divergent non-canonical NF-κB pathway in the context of pancreatic islet dysfunction in diabetes. Here, we demonstrate that pharmacological activation of the non-canonical NF-κB inducing kinase (NIK) disrupts glucose homeostasis in zebrafish in vivo. Further, we identify NIK as a critical negative regulator of beta cell function as pharmacological NIK activation results in impaired glucose-stimulated insulin secretion in mouse and human islets. NIK levels are elevated in pancreatic islets isolated from diet-induced obese (DIO) mice, which exhibit increased processing of non-canonical NF-κB components p100 to p52, and accumulation of RelB. Tumor necrosis factor α (TNFα) and receptor activator of NF-κB ligand (RANKL), two ligands associated with diabetes, induce NIK in islets. Mice with constitutive beta cell intrinsic NIK activation present impaired insulin secretion with DIO. NIK activation triggers the non-canonical NF-κB transcriptional network to induce genes identified in human type 2 diabetes genome-wide association studies linked to beta cell failure. These studies reveal that NIK contributes a central mechanism for beta cell failure in diet-induced obesity. We identify a role for Nuclear Factor inducing κB (NIK) in pancreatic beta cell failure. NIK activation disrupts glucose homeostasis in zebrafish in vivo and impairs glucose-stimulated insulin secretion in mouse and human islets in vitro. NIK activation also perturbs beta cell insulin secretion in a diet-induced obesity mouse model. These studies reveal that NIK contributes a central mechanism for beta cell failure in obesity. To uncover the role of NIK in pancreatic beta cells, we performed a gene expression microarray analysis comparing pancreatic islets with constitutive beta cell intrinsicNIK activation from the 16 week old mice (beta cell specific TRAF2 and TRAF2 knockout mice) to their controls (n=3 per group).
2015-06-18 | E-GEOD-68317 | biostudies-arrayexpress
Project description:The Nuclear Immune Receptor RPS4 Is Required for RRS1SLH1-Dependent Constitutive Defense Activation in Arabidopsis thaliana.
| PRJNA209363 | ENA
Project description:The Nuclear Immune Receptor RPS4 Is Required for RRS1SLH1-Dependent Constitutive Defense Activation in Arabidopsis thaliana.
| PRJNA221223 | ENA
Project description:To generate an efficient defense against begomovirus, we modulated the activity of the immune defense receptor NIK (NSP-Interacting Kinase) in tomato plants; NIK is a virulence target of the begomovirus NSP during infection. Replacing threonine-474 with aspartate (T474D) within the kinase activation loop promoted the constitutive activation of NIK-mediated defenses. This activation resulted in the down-regulation of translation-related genes and the suppression of global translation in T474D-overexpressing tomato lines. We also found that T474D-induced defense-related transcripts were associated with polysomes and immune proteins, which accumulated to detectable levels in T474D leaves. Consistent with these findings, T474D transgenic lines were tolerant to the tomato-infecting begomoviruses ToYSV and ToSRV. We propose that NIK mediates an anti-viral response via translation suppression and immune system induction.
2013-12-17 | GSE38028 | GEO
Project description:The NF-κB pathway is a master regulator of inflammatory processes and is implicated in insulin resistance and pancreatic beta cell dysfunction in the metabolic syndrome. While canonical NF-κB signaling is well studied, there is little information on the divergent non-canonical NF-κB pathway in the context of pancreatic islet dysfunction in diabetes. Here, we demonstrate that pharmacological activation of the non-canonical NF-κB inducing kinase (NIK) disrupts glucose homeostasis in zebrafish in vivo. Further, we identify NIK as a critical negative regulator of beta cell function as pharmacological NIK activation results in impaired glucose-stimulated insulin secretion in mouse and human islets. NIK levels are elevated in pancreatic islets isolated from diet-induced obese (DIO) mice, which exhibit increased processing of non-canonical NF-κB components p100 to p52, and accumulation of RelB. Tumor necrosis factor α (TNFα) and receptor activator of NF-κB ligand (RANKL), two ligands associated with diabetes, induce NIK in islets. Mice with constitutive beta cell intrinsic NIK activation present impaired insulin secretion with DIO. NIK activation triggers the non-canonical NF-κB transcriptional network to induce genes identified in human type 2 diabetes genome-wide association studies linked to beta cell failure. These studies reveal that NIK contributes a central mechanism for beta cell failure in diet-induced obesity. We identify a role for Nuclear Factor inducing κB (NIK) in pancreatic beta cell failure. NIK activation disrupts glucose homeostasis in zebrafish in vivo and impairs glucose-stimulated insulin secretion in mouse and human islets in vitro. NIK activation also perturbs beta cell insulin secretion in a diet-induced obesity mouse model. These studies reveal that NIK contributes a central mechanism for beta cell failure in obesity.
2015-06-18 | GSE68317 | GEO
Project description:Genomic copy number variation induced by TAQing system in Arabidopsis thaliana.
| PRJNA354554 | ENA