Project description:in this work, initially we ectopically expressed the legume Nod factor receptor genes (NFRP genes – MtNFP, MtLYK3 and LjLNP) in rice and assessed their impact on NF perception and consequently-triggered biological processes in roots. RNA-seq transcriptomic analysis revealed that the ectopic expression of the legume NFRPs in roots suppressed diverse genes associated with plant pathogen interaction and other defense response pathways including the ones involved in secondary metabolism. Overall, results the study indicate that (1) rice (control) plants have inherent ability to perceive NFs, and the perception of NFs resulted in suppression of a significant number of genes involved in innate immune response in roots; (2) Ectopic expression of NFRPs primed root hairs to respond to NFs; and (3) Expression of NFRPs made rice roots hypersensitive to NFs, as they triggered massive up-regulation of diverse defense response and secondary metabolism genes.
Project description:NGS2013-04: Transcriptomic response to Nod Factor treatments on Medicago Role of the root hair in water and nutrient uptake and the establishment of the nitrogen-fixing symbiotic interaction with rhizobia. The RNA was extracted from root hairs of Medicago: control vs treated by nod factors (2 biological replicates)
Project description:NGS2013-04: Transcriptomic response to Nod Factor treatments on Medicago Role of the root hair in water and nutrient uptake and the establishment of the nitrogen-fixing symbiotic interaction with rhizobia.
Project description:With the goal of identifying changes in gene expression in CD4(+) T cells during the development of diabetes in the nonobese diabetic (NOD) mouse, we used DNA microarrays to analyze gene expression in CD4(+) T cells from the pancreatic draining lymph nodes of NOD/BDC 2.5 T cell receptor transgenic and WT NOD mice at different ages. At 4 and 6 weeks of age, we found up-regulation of a number of genes that are known to be induced by IFN-alpha. IFN-alpha levels and IFN-alpha-producing plasmacytoid dendritic cells were increased in the PLNs of 3- to 4-week-old NOD mice. Moreover, blockade of IFN-alpha receptor 1 in NOD mice by a neutralizing antibody at 2-3 weeks of age significantly delayed the onset and decreased the incidence of type 1 diabetes, increased the relative number of immature dendritic cells in the PLNs, and enhanced the ability of spleen CD4(+) T cells to produce IL-4 and IL-10. These findings demonstrate that IFN-alpha in the PLNs is an essential initiator in the pathogenesis of type 1 diabetes in NOD mice.
Project description:This experiment was part of a larger study to elucidate the early effects of Nod factor treatment on the Medicago truncatula phosphoproteome, transcriptome and metabolome in wildtype and two mutants. In this experiment, RNA-Seq was used to measure transcriptional changes in plant roots treated +/- Nod factors for 1 hr. All plants were treated for one hour by replacement of the medium with modified Fahraeus medium with and without 10â8 molar Nod factors obtained from Sinorhizobium meliloti strain Rm1021 pRmE43 (pTE3:nodD1). Seedlings were harvested after one hour of treatment. RNA was extracted and sequenced from three biological replicates of each treatment condition in wildtype as well as mutants in nfp and dmi3, two genes known to be involved in the response pathway.
Project description:Currently unpublished data suggested that the foliar application of the Bradyrhizobium japonicum Nod factor induced changes in hormone level and enzyme activity in soybean cv. OAC Bayfield. This study was designed to examine any possible differences in gene expression that occur as a result of the foliar treatment of Nod factor. The data herein are gene expression data of that experiment, from the sprayed, first trifoliolate leaf of each plant, 48 h after treatment. Keywords: stress response
Project description:Currently unpublished data suggested that the foliar application of the Bradyrhizobium japonicum Nod factor induced changes in hormone level and enzyme activity in soybean cv. OAC Bayfield. This study was designed to examine any possible differences in gene expression that occur as a result of the foliar treatment of Nod factor. The data herein are gene expression data of that experiment, from the sprayed, first trifoliolate leaf of each plant, 48 h after treatment. Experiment Overall Design: This experimental design was a Completely Randomized Design (CRD), comparing 1 treatment (first trifoliolate leaf sprayed with 10^-7M LCO/Nod factor and 0.02% Tween 20) against a mock-treated control (first trifoliolate leaf sprayed with dH2O and 0.02% Tween 20). There are 3 replicates per treatment type, with a total of 6 samples for this experiment.
Project description:With the goal of identifying changes in gene expression in CD4(+) T cells during the development of diabetes in the nonobese diabetic (NOD) mouse, we used DNA microarrays to analyze gene expression in CD4(+) T cells from the pancreatic draining lymph nodes of NOD/BDC 2.5 T cell receptor transgenic and WT NOD mice at different ages. At 4 and 6 weeks of age, we found up-regulation of a number of genes that are known to be induced by IFN-alpha. IFN-alpha levels and IFN-alpha-producing plasmacytoid dendritic cells were increased in the PLNs of 3- to 4-week-old NOD mice. Moreover, blockade of IFN-alpha receptor 1 in NOD mice by a neutralizing antibody at 2-3 weeks of age significantly delayed the onset and decreased the incidence of type 1 diabetes, increased the relative number of immature dendritic cells in the PLNs, and enhanced the ability of spleen CD4(+) T cells to produce IL-4 and IL-10. These findings demonstrate that IFN-alpha in the PLNs is an essential initiator in the pathogenesis of type 1 diabetes in NOD mice. An all pairs experiment design type is where all labeled extracts are compared to every other labeled extract.
Project description:Signaling via the intracellular pathogen receptors Nucleotide-binding oligomerization domain-containing proteins NOD1 and NOD2 requires Receptor Interacting Kinase 2 (RIPK2), an adaptor kinase that can be targeted for the treatment of various inflammatory diseases. However, the molecular mechanisms of how RIPK2 contributes to NOD signaling are not completely understood. We generated FLAG-tagged RIPK2 knock-in mice using CRISPR/Cas9 technology to study NOD signaling mechanisms on an endogenous level. Using cells from these mice we were able to generate a detailed map of post-translational modifications on RIPK2 during NOD signaling using mass spectrometry analysis and we identified a new regulatory interface on RIPK2, which dictates the crucial interaction with the E3 ligase XIAP.
Project description:Total pancreatic RNA was isolated from 3 week old NOD.scid, NOD, BDC2.5/NOD and BDC2.5/NOD.scid animals by GITC method. Targets were produced using standard Affymetrix procedures from about 10ug total RNA. The data from NOD.scid, NOD, BDC2.5/NOD and BDC2.5/NOD.scid Affymetrix MGU74Av2 cel files was converted into Robust Multi Array (RMA) text file for analysis using GeneSpring 6.1 Keywords: other