Comparison of low water potential (drought) regulated gene expression in wild type (Col-0) and egr1-1egr2-1 (At3g05640/At5g27930) mutant.
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ABSTRACT:
ORGANISM(S): Arabidopsis thaliana
PROVIDER: GSE71237 | GEO | 2015/10/08
SECONDARY ACCESSION(S): PRJNA290646
REPOSITORIES: GEO
Similar Datasets
Project description:I-Traq based quantitative phosphoproteomics was used to examine changes in phosphopeptide abundance over longer term drought (low water potential) treatments. Samples were analyzed from unstressed seedlings grown on agar plates and from seedlings of the same age that had been transferred to low water potential (-1.2 MPa) for 96 h on PEG-infused agar plates. The genotypes analyzed were wild type Col-0 and two phosphatases mutants. One was a double mutant of two Clade E protein phosphatase 2Cs (Salk_011589 which lacks activity of AT3G05640 and Salk_048861 which lacks activity of AT5G27930). The other was a mutant (hai1-2) of the Clade A protein phosphatase 2C Highly ABA-Induced 1 (HAI1): Salk_108282 which lacks activity of AT5G59220). Our characterization of hai1-2 as well as detailed description of growth conditions and stress treatments has been reported in Bhaskara et al. (Plant Physiology 160:379-395, 2012). Characterization of the Clade E protein phosphatase 2Cs have not been previously reported and we have designated these as Clade E Growth Regulating PP2Cs (EGRs) based on characterization in our laboratory. The double mutant used for phosphoproteomic analysis has been designated egr1-1egr2-1. Three biological replicates were performed and microarray analysis of gene expression was performed on samples collected from the same experiments. The gene expression data sets have been deposited in Gene Expression Onmibus (GEO) under accession numbers GSE35258 (hai1-2 data) and GSE71237 (egr1-1egr2-1 data).
2017-01-17 | PXD004869 | Pride
Project description:The early growth response (Egr) family of transcriptional regulators consists of four closely related molecules (Egr1-4) that regulate target genes involved in cellular growth and differentiation. In the brain, Egr transcription factors have a critical role in learning and memory processing, presumably by regulating effector target genes that alter synaptic efficacy or mediate structural changes in neurons. Previous work suggests that Egr1 and Egr3 are the most important synaptic activity induced Egr molecules in the brain and they appear to have redundant regulatory function. How Egr transcriptional regulators influence learning and memory processing in the brain is unknown because target genes regulated by them have not been identified. Using Affymetrix microarray analysis and Egr loss-of-function mice, we will begin to characterize the gene regulatory networks modulated by Egr transcription factors in the brain. We anticipate that basic mechanisms related to transcriptional control of learning and memory related plasticity and the identification of plasticity effector molecules that may be involved in synaptic dysfunction associated with degenerative diseases or brain injury will result from these studies. To identify Egr transcription factor target gene regulation in brain: Target genes regulated by Egr transcription factors have not been identified in the brain, yet the transcription factors are essential for normal learning and memory processes. Using Egr1/3 double knockout and wild type littermate mice, we will compare gene expression profiles from somatosensory cortex to identify genes that are deregulated in Egr1/3 dKO brains. Egr1 and Egr3 gene expression is coupled to synaptic N-methyl D-aspartate (NMDA) receptor activation, mitogen activated protein kinase (MAPK) signaling engaged by NMDA receptor activation and long term synaptic potentiation (LTP). Previous studies have demonstrated defects in late phase LTP, long-term memory in hippocampal dependent tasks and reconsolidation of memories in Egr1-deficient mice, but the target effector molecules regulated by Egr transcription factors are not known. We hypothesize that it will be possible to identify Egr dependent target genes by using Affymetrix microarray analysis to compare gene expression from wild type cerebral cortex that has high levels of Egr protein expression with gene expression in cortex from Egr1/3 double knockout mice. Egr1 and Egr3 are highly expressed in mouse cortex and hippocampus twenty one days after birth because of the large amount of maternal stimulation they receive prior to weaning. We will compare the gene expression profile in somatosensory cortex from P21 wild type mice to that of P21 Egr1/3 dKO mice. We will perform microarray analysis using the Mouse 430 2.0 gene array with RNA samples from 3 wild type and 3 1/3 dKO brains (6 arrays total). Differentially regulated genes (up-regulated and down-regulated) will be identified from the list of genes with significantly altered expression greater than or equal to 2-fold by paired T test. Interesting genes will be validated by real-time PCR in wild type and 1/3 dKO brains. Our main goal is to identify genes that are directly regulated by Egr3. Recognizing that both direct and indirect target genes may be identified in the list of differentially expressed genes, real-time PCR validated target genes will be further screened using chromatin immunoprecipitation coupled with PCR (ChIP-PCR) to determine whether Egr1 and/or Egr3 are bound to potential regulatory regions of the putative target genes.
2008-06-13 | E-GEOD-4752 | biostudies-arrayexpress
Project description:The Clade A PP2C Highly ABA-Induced1 (HAI1, At5g59220) is strongly up-regulated by low water potential in an ABA-dependent manner. Using knockout mutants of hai1, we found that HAI1 functions as a negative regulator of low water potential-induced proline and osmoregulatory solute accumulation. We also found a relatively weak and limited interaction of HAI1 with the RCAR/PYL family of ABA receptors. This, plus its induced expression, suggest that HAI1 remains active during stress and attenuates specific aspects of drought response. Microarray experiments were used to identify genes differentially expressed in hai1-2 (SALK_108282) versus wild type under both unstress control conditions and after low water potential (i.e., drought, water deficit). A relatively long term (96 h) low water potential treatment was used as phenotypes of hai1-2 were most apparent after this longer term low water potential treatment.
2012-02-03 | GSE35258 | GEO
Project description:The early growth response (Egr) family of transcriptional regulators consists of four closely related molecules (Egr1-4) that regulate target genes involved in cellular growth and differentiation. In the brain, Egr transcription factors have a critical role in learning and memory processing, presumably by regulating effector target genes that alter synaptic efficacy or mediate structural changes in neurons. Previous work suggests that Egr1 and Egr3 are the most important synaptic activity induced Egr molecules in the brain and they appear to have redundant regulatory function. How Egr transcriptional regulators influence learning and memory processing in the brain is unknown because target genes regulated by them have not been identified. Using Affymetrix microarray analysis and Egr loss-of-function mice, we will begin to characterize the gene regulatory networks modulated by Egr transcription factors in the brain. We anticipate that basic mechanisms related to transcriptional control of learning and memory related plasticity and the identification of plasticity effector molecules that may be involved in synaptic dysfunction associated with degenerative diseases or brain injury will result from these studies. To identify Egr transcription factor target gene regulation in brain: Target genes regulated by Egr transcription factors have not been identified in the brain, yet the transcription factors are essential for normal learning and memory processes. Using Egr1/3 double knockout and wild type littermate mice, we will compare gene expression profiles from somatosensory cortex to identify genes that are deregulated in Egr1/3 dKO brains. Egr1 and Egr3 gene expression is coupled to synaptic N-methyl D-aspartate (NMDA) receptor activation, mitogen activated protein kinase (MAPK) signaling engaged by NMDA receptor activation and long term synaptic potentiation (LTP). Previous studies have demonstrated defects in late phase LTP, long-term memory in hippocampal dependent tasks and reconsolidation of memories in Egr1-deficient mice, but the target effector molecules regulated by Egr transcription factors are not known. We hypothesize that it will be possible to identify Egr dependent target genes by using Affymetrix microarray analysis to compare gene expression from wild type cerebral cortex that has high levels of Egr protein expression with gene expression in cortex from Egr1/3 double knockout mice. Egr1 and Egr3 are highly expressed in mouse cortex and hippocampus twenty one days after birth because of the large amount of maternal stimulation they receive prior to weaning. We will compare the gene expression profile in somatosensory cortex from P21 wild type mice to that of P21 Egr1/3 dKO mice. We will perform microarray analysis using the Mouse 430 2.0 gene array with RNA samples from 3 wild type and 3 1/3 dKO brains (6 arrays total). Differentially regulated genes (up-regulated and down-regulated) will be identified from the list of genes with significantly altered expression greater than or equal to 2-fold by paired T test. Interesting genes will be validated by real-time PCR in wild type and 1/3 dKO brains. Our main goal is to identify genes that are directly regulated by Egr3. Recognizing that both direct and indirect target genes may be identified in the list of differentially expressed genes, real-time PCR validated target genes will be further screened using chromatin immunoprecipitation coupled with PCR (ChIP-PCR) to determine whether Egr1 and/or Egr3 are bound to potential regulatory regions of the putative target genes. Keywords: other
2006-05-02 | GSE4752 | GEO
Project description:The Early Growth Response (Egr) family of transcription factors consists of 4 members (Egr1-4) that are expressed in a wide variety of cell types. A large body of evidence point to a role for Egr transcription factors in growth, survival, and differentiation. A major unanswered question is whether Egr transcription factors serve similar functions in diverse cell types by activating a common set of target genes. Signal transduction cascades in neurons and lymphocytes show striking parallels. Activation of either cell type activates the Ras-MAPK pathway and, in parallel, leads to increases in intracellular calcium stimulating the calcineurin-NFAT pathway. In both cell types, the strength of the activation signal affects the cellular outcomes and very strong stimuli lead to cell death. Notably both these pathways converge on the induction of Egr genes. We believe that downstream targets of Egr transcription factors in lymphocytes may also be activated by Egr factors in activated neurons. There is precedence for common target gene activation in these two cell types: apoptosis in both activated T cells and methamphetamine stimulated neurons occurs via FasL induction by NFAT transcription factors. We propose to use developing T lymphocytes (thymocytes) as a model system for discovery of Egr-dependent target genes for several reasons. First, we have observed a prominent survival defect in thymocytes from mice deficient in both Egr1 and Egr3 (1/3 DKO) and a partial differention block in the immature double negative (DN) stage. In addition, thymocytes are an easily manipulatable cell type, and the DN subpopulation affected in 1/3 DKO mice can be isolated to very high purity. We anticipate that 1/3 DKO thymocytes will provide an excellent experimental system that will provide insight into Egr-dependent transcription in neuronal development, activation, and death. To identify Egr transcription factor target genes in developing thymocytes. Egr1/3 DKO mice show a profound defect in thymocyte survival and differentiation, but the target genes downstream of Egr1 and Egr3 are unknown. Using Egr1/3 double knockout and wild type littermate mice, we will compare gene expression profiles from DN thymocytes to identify genes that are deregulated in Egr1/3 DKO cells. Egr1 and Egr3 expression is necessary for the proper survival and differentiation of developing thymocytes. We hypothesize that we will be able to identify crucial target genes of Egr1 and Egr3 by comparing gene expression profiles from wild type and 1/3 DKO thymocytes. Egr1 and Egr3 are first expressed in the immature double negative (DN) thymocytes. We will isolate DN thymocytes by FACS sorting which allows isolation of cell populations of >99% purity. We will perform microarray analysis using the Mouse 430 2.0 gene array with thymocyte RNA samples from 3 wild type and 3 1/3 DKO mice (6 arrays total). Differentially regulated genes (up-regulated and down-regulated) will be identified from the list of genes with significantly altered expression greater than or equal to 2-fold by paired T test. Interesting genes will be validated by real-time PCR in wild type and 1/3 DKO thymocytes. Recognizing that both direct and indirect target genes may be identified in the list of differentially expressed genes, real-time PCR validated target genes will be further screened using chromatin immunoprecipitation coupled with PCR (ChIP-PCR) to determine whether Egr1 and/or Egr3 are bound to potential regulatory regions of the putative target genes.
2008-06-13 | E-GEOD-5587 | biostudies-arrayexpress
Project description:The Clade A PP2C Highly ABA-Induced1 (HAI1, At5g59220) is strongly up-regulated by low water potential in an ABA-dependent manner. Using knockout mutants of hai1, we found that HAI1 functions as a negative regulator of low water potential-induced proline and osmoregulatory solute accumulation. We also found a relatively weak and limited interaction of HAI1 with the RCAR/PYL family of ABA receptors. This, plus its induced expression, suggest that HAI1 remains active during stress and attenuates specific aspects of drought response. Microarray experiments were used to identify genes differentially expressed in hai1-2 (SALK_108282) versus wild type under both unstress control conditions and after low water potential (i.e., drought, water deficit). A relatively long term (96 h) low water potential treatment was used as phenotypes of hai1-2 were most apparent after this longer term low water potential treatment. Seven-day-old seedlings of wild type (Col-0) or hai1-2 were transferred from agar plates of control media to low water potential stress (PEG-infused agar plates at -1.2 MPa) or to fresh control media (-0.25 Mpa). Samples (whole seedlings) were collected 96 h after transfer. Three independent experiments were conducted with one sample of each treatment (wild type stress and control, hai1-2 stress and control) collected from each experiment.
2012-02-03 | E-GEOD-35258 | biostudies-arrayexpress
Project description:Nerve growth factor (NGF) is a neurotrophin that plays an important role in regulating the survival, growth, and differentiation of sympathetic neurons. Many in vitro studies indicate that Egr transcription factors are coupled to NGF signaling and are essential signaling mediators of NGF-dependent differentiation of sympathetic neurons, such as neuroblastoma cells and pheochromocytoma cells. Mice that are deficient for both Egr1 and Egr3 have profound sympathetic nerve system defects, including abnormal neuron degeneration and impaired differentiation (unpublished observations). To further understand the role of Egr genes in sympathetic neuron development, it is necessary to examine the signal transduction pathways involved in NGF-mediated Egr-dependent gene regulation. The results will be helpful in understanding the pathobiology of those diseases related to aberrant sympathetic neuron differentiation, such as neuroblastoma and dysautonomias, and may provide new insights into therapies for these refractory diseases. To identify NGF-mediated Egr-dependent target genes in human SH-SY5Y/TrkA neuroblastoma cells: Many potential Egr target genes have been described over the years. However, very few have been characterized to be involved in NGF-mediated sympathetic neuron differentiation. In order to further understand the role of Egr genes in sympathetic neuron development, it is necessary to examine the signal transduction pathways involved in NGF-mediated Egr-dependent gene regulation. Egr1 and Egr3 are rapidly induced after NGF treatment and Egr1 is involved in activation of the differentiation marker gene NPY in SH-SY5Y/TrkA cells. Therefore, SH-SY5Y/TtrkA cells appear to be an excellent model system to study the role of Egr transcription factors in sympathetic neuron differentiation in vitro. A dominant negative Egr molecule that specifically blocks transcriptional activity mediated by Egr transcription factors will be used in this study to identify Egr-dependent target genes. Egr1 and Egr3 are rapidly induced after NGF treatment in human SH-SY5Y/TrkA neuroblastoma cells, which in turn differentiate into sympathetic-like neurons. We hypothesize that Egr transcription factors are involved in activating downstream signaling pathways during NGF mediated differentiation of SH-SY5Y/TrkA cells. Moreover, we hypothesize that by using a dominant negative Egr (dnEgr) molecule that blocks all Egr mediated gene transcription and Affymetrix microarray analysis, it will be possible to identify NGF-mediated Egr transcription dependent gene regulatory networks that may be involved in growth and differentiation of neuroblastoma. An unbiased approach to understanding these gene regulatory networks may lead to new insights relating to NGF signaling involved in neuronal growth and differentiation. Human neuroblastoma SH-SY5Y/TrkA cells will be infected with either dnEgr-expressing adenovirus (SH-SY5Y/TrkA-dnEgr) or with EGFP-expressing control adenovirus (SH-SY5Y/TrkA-EGFP). Equivalent infection efficiency and lack of viral toxicity will be verified by EGFP fluorescence microscopy 24 hours after infection and the cells will be treated with NGF (100 ng/ml). Total RNA will be extracted from SH-SY5Y/TrkA (uninfected), SH-SY5Y/TrkA-dnEgr, and SH-SY5Y/TrkA-EGFP cells treated with NGF for 0, 1 hour and 3 hours. Total RNA will be prepared from all of the samples and a portion subjected to real-time PCR analysis to ensure that NGF mediated Egr gene induction was not altered by the context of viral infection. Pilot experiments demonstrate that Egr genes are still induced in the context of viral infection greater than 100-fold. Egr1 mRNA peak expression is known to occur at 1 hour and decrease by 3 hours after NGF treatment in all of the samples. The peak expression of Egr target genes is expected to occur later than Egr1 peak expression since Egr1 proteins need to be expressed first to initiate the transcription of target promoters. Therefore, the RNA samples from SH-SY5Y/TrkA-dnEgr and SH-SY5Y/TrkA-EGFP treated with NGF for 3 hours will be used to probe Affymetrix high-density human genome U133 Plus 2.0 Arrays to identify differentially expressed genes. RNA amplification for probe synthesis should not be necessary since we will provide 10 ug of intact total RNA for each sample. We will provide three sets of samples to perform the comparative microarray analysis twice from different starting materials and a nine-way comparative analysis of the data will be performed. We expect that cells containing high levels of dnEgr will inhibit NGF mediated Egr-dependent target gene expression and that these gene networks should be identifiable when compared to EGFP infected cells that have normal Egr gene transcriptional activity. Experiment Overall Design: as above
2008-06-12 | E-GEOD-2864 | biostudies-arrayexpress
Project description:The Early Growth Response (Egr) family of transcription factors consists of 4 members (Egr1-4) that are expressed in a wide variety of cell types. A large body of evidence point to a role for Egr transcription factors in growth, survival, and differentiation. A major unanswered question is whether Egr transcription factors serve similar functions in diverse cell types by activating a common set of target genes. Signal transduction cascades in neurons and lymphocytes show striking parallels. Activation of either cell type activates the Ras-MAPK pathway and, in parallel, leads to increases in intracellular calcium stimulating the calcineurin-NFAT pathway. In both cell types, the strength of the activation signal affects the cellular outcomes and very strong stimuli lead to cell death. Notably both these pathways converge on the induction of Egr genes. We believe that downstream targets of Egr transcription factors in lymphocytes may also be activated by Egr factors in activated neurons. There is precedence for common target gene activation in these two cell types: apoptosis in both activated T cells and methamphetamine stimulated neurons occurs via FasL induction by NFAT transcription factors. We propose to use developing T lymphocytes (thymocytes) as a model system for discovery of Egr-dependent target genes for several reasons. First, we have observed a prominent survival defect in thymocytes from mice deficient in both Egr1 and Egr3 (1/3 DKO) and a partial differention block in the immature double negative (DN) stage. In addition, thymocytes are an easily manipulatable cell type, and the DN subpopulation affected in 1/3 DKO mice can be isolated to very high purity. We anticipate that 1/3 DKO thymocytes will provide an excellent experimental system that will provide insight into Egr-dependent transcription in neuronal development, activation, and death. To identify Egr transcription factor target genes in developing thymocytes. Egr1/3 DKO mice show a profound defect in thymocyte survival and differentiation, but the target genes downstream of Egr1 and Egr3 are unknown. Using Egr1/3 double knockout and wild type littermate mice, we will compare gene expression profiles from DN thymocytes to identify genes that are deregulated in Egr1/3 DKO cells. Egr1 and Egr3 expression is necessary for the proper survival and differentiation of developing thymocytes. We hypothesize that we will be able to identify crucial target genes of Egr1 and Egr3 by comparing gene expression profiles from wild type and 1/3 DKO thymocytes. Egr1 and Egr3 are first expressed in the immature double negative (DN) thymocytes. We will isolate DN thymocytes by FACS sorting which allows isolation of cell populations of >99% purity. We will perform microarray analysis using the Mouse 430 2.0 gene array with thymocyte RNA samples from 3 wild type and 3 1/3 DKO mice (6 arrays total). Differentially regulated genes (up-regulated and down-regulated) will be identified from the list of genes with significantly altered expression greater than or equal to 2-fold by paired T test. Interesting genes will be validated by real-time PCR in wild type and 1/3 DKO thymocytes. Recognizing that both direct and indirect target genes may be identified in the list of differentially expressed genes, real-time PCR validated target genes will be further screened using chromatin immunoprecipitation coupled with PCR (ChIP-PCR) to determine whether Egr1 and/or Egr3 are bound to potential regulatory regions of the putative target genes. Keywords: other
2006-08-24 | GSE5587 | GEO
Project description:Nerve growth factor (NGF) is a neurotrophin that plays an important role in regulating the survival, growth, and differentiation of sympathetic neurons. Many in vitro studies indicate that Egr transcription factors are coupled to NGF signaling and are essential signaling mediators of NGF-dependent differentiation of sympathetic neurons, such as neuroblastoma cells and pheochromocytoma cells. Mice that are deficient for both Egr1 and Egr3 have profound sympathetic nerve system defects, including abnormal neuron degeneration and impaired differentiation (unpublished observations). To further understand the role of Egr genes in sympathetic neuron development, it is necessary to examine the signal transduction pathways involved in NGF-mediated Egr-dependent gene regulation. The results will be helpful in understanding the pathobiology of those diseases related to aberrant sympathetic neuron differentiation, such as neuroblastoma and dysautonomias, and may provide new insights into therapies for these refractory diseases. To identify NGF-mediated Egr-dependent target genes in human SH-SY5Y/TrkA neuroblastoma cells: Many potential Egr target genes have been described over the years. However, very few have been characterized to be involved in NGF-mediated sympathetic neuron differentiation. In order to further understand the role of Egr genes in sympathetic neuron development, it is necessary to examine the signal transduction pathways involved in NGF-mediated Egr-dependent gene regulation. Egr1 and Egr3 are rapidly induced after NGF treatment and Egr1 is involved in activation of the differentiation marker gene NPY in SH-SY5Y/TrkA cells. Therefore, SH-SY5Y/TtrkA cells appear to be an excellent model system to study the role of Egr transcription factors in sympathetic neuron differentiation in vitro. A dominant negative Egr molecule that specifically blocks transcriptional activity mediated by Egr transcription factors will be used in this study to identify Egr-dependent target genes. Egr1 and Egr3 are rapidly induced after NGF treatment in human SH-SY5Y/TrkA neuroblastoma cells, which in turn differentiate into sympathetic-like neurons. We hypothesize that Egr transcription factors are involved in activating downstream signaling pathways during NGF mediated differentiation of SH-SY5Y/TrkA cells. Moreover, we hypothesize that by using a dominant negative Egr (dnEgr) molecule that blocks all Egr mediated gene transcription and Affymetrix microarray analysis, it will be possible to identify NGF-mediated Egr transcription dependent gene regulatory networks that may be involved in growth and differentiation of neuroblastoma. An unbiased approach to understanding these gene regulatory networks may lead to new insights relating to NGF signaling involved in neuronal growth and differentiation. Human neuroblastoma SH-SY5Y/TrkA cells will be infected with either dnEgr-expressing adenovirus (SH-SY5Y/TrkA-dnEgr) or with EGFP-expressing control adenovirus (SH-SY5Y/TrkA-EGFP). Equivalent infection efficiency and lack of viral toxicity will be verified by EGFP fluorescence microscopy 24 hours after infection and the cells will be treated with NGF (100 ng/ml). Total RNA will be extracted from SH-SY5Y/TrkA (uninfected), SH-SY5Y/TrkA-dnEgr, and SH-SY5Y/TrkA-EGFP cells treated with NGF for 0, 1 hour and 3 hours. Total RNA will be prepared from all of the samples and a portion subjected to real-time PCR analysis to ensure that NGF mediated Egr gene induction was not altered by the context of viral infection. Pilot experiments demonstrate that Egr genes are still induced in the context of viral infection greater than 100-fold. Egr1 mRNA peak expression is known to occur at 1 hour and decrease by 3 hours after NGF treatment in all of the samples. The peak expression of Egr target genes is expected to occur later than Egr1 peak expression since Egr1 proteins need to be expressed first to initiate the transcription of target promoters. Therefore, the RNA samples from SH-SY5Y/TrkA-dnEgr and SH-SY5Y/TrkA-EGFP treated with NGF for 3 hours will be used to probe Affymetrix high-density human genome U133 Plus 2.0 Arrays to identify differentially expressed genes. RNA amplification for probe synthesis should not be necessary since we will provide 10 ug of intact total RNA for each sample. We will provide three sets of samples to perform the comparative microarray analysis twice from different starting materials and a nine-way comparative analysis of the data will be performed. We expect that cells containing high levels of dnEgr will inhibit NGF mediated Egr-dependent target gene expression and that these gene networks should be identifiable when compared to EGFP infected cells that have normal Egr gene transcriptional activity. Keywords: time-course
2005-07-06 | GSE2864 | GEO
Project description:EGR2 is an early growth response transcription factor that negatively regulates T-cell activation, in contrast to its positive regulation by EGR1. Here, we unexpectedly found that EGR2 promotes peripheral naïve T cell differentiation, with delayed TCR-induced proliferation in naïve T cells from Egr2 conditional knockout (CKO) mice, and decreased production of IFN-γ, IL-4, IL-9, and IL-17A in cells subjected to T helper differentiation. Moreover, genes that promote T-cell activation, including Tbx21 and Notch1, had decreased expression in Egr2 CKO T cells and are direct EGR2 target genes. Following influenza infection, Egr2 CKO mice had delayed viral clearance, more weight loss, and more severe pathological changes in the lung than did WT and Egr1 KO mice, with decreased production of effector cytokines and infiltration of antigen-specific memory-precursor CD8+ T cells but lower numbers of lung-resident memory CD8+ T cells. Thus unexpectedly EGR2 can function as a positive regulator that is essential for naïve T-cell differentiation and in vivo T-cell responses to a viral infection.
2014-10-21 | GSE49366 | GEO