Transcription profiling of mouse bone marrow derived macrophages (BMDM) treated with anthrax edema toxin (ET)
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ABSTRACT: Bacillus anthracis, the causative agent of anthrax, secretes three toxin proteins: protective antigen (PA), lethal factor (LF), and edema factor (EF). PA is a transporter of LF and EF into host cells by receptor-mediated endocytosis. LF is a metalloprotease that cleaves mitogen-activated protein kinase (MAPK) kinases (MKK), while EF is an adenylate cyclase, which converts ATP to cAMP. We used microarrays to decipher the specific gene regulation in edema toxin (ET), the complex of EF and PA, treated mouse bone marrow derived macrophages. Experiment Overall Design: BMDM were treated with 1 mg/ml of ET and the RNAs were purified at 0, 2, and 4h after toxin treatment.
Project description:Bacillus anthracis, the causative agent of anthrax, secretes three toxin proteins: protective antigen (PA), lethal factor (LF), and edema factor (EF). PA is a transporter of LF and EF into host cells by receptor-mediated endocytosis. LF is a metalloprotease that cleaves mitogen-activated protein kinase (MAPK) kinases (MKK), while EF is an adenylate cyclase, which converts ATP to cAMP. We used microarrays to decipher the specific gene regulation in edema toxin (ET), the complex of EF and PA, treated mouse bone marrow derived macrophages. Keywords: Time course
Project description:Edema toxin (EdTx), which is a combination of edema factor and a binding moiety (protective antigen), is produced by Bacillus anthracis, the etiological agent of anthrax. EdTx is an adenylyl cyclase enzyme that converts adenosine triphosphate to adenosine-3',5'-monophosphate, resulting in interstitial edema seen in anthrax patients. We used GeneChip analysis to examine global transcriptional profiles of EdTx-treated RAW 264.7 murine macrophage-like cells at 3 and 6 hr. Experiment Overall Design: RAW 264.7 cells were treated with EdTx (2.5 µg/ml of protective antigen and 0.625 µg/ml of Edema factor), PA (2.5 µg/ml), or LPS (1 ng/mL) for 0, 3, and 6 hr. Each experiment was performed in triplicate, generating a total of 21 arrays (biological replciates).
Project description:Edema toxin (EdTx), which is a combination of edema factor and a binding moiety (protective antigen), is produced by Bacillus anthracis, the etiological agent of anthrax. EdTx is an adenylyl cyclase enzyme that converts adenosine triphosphate to adenosine-3’,5’-monophosphate, resulting in interstitial edema seen in anthrax patients. We used GeneChip analysis to examine global transcriptional profiles of EdTx-treated RAW 264.7 murine macrophage-like cells at 3 and 6 hr. Keywords: Toxin response
Project description:We found that intrathecal injection of anthrax edema toxin (ET), causes analgesia in adult B6J mice. In order to determine if DRG neuron transcriptional responses play a role in pain blockade, we performed a bulk RNA-seq experiment on dissected mouse DRG neurons. We report that anthrax edema toxin causes transcriptional responses in DRG neurons 2h after in vivo administration
Project description:The activity of known anthrax toxins is insufficient to account the effects on functions of hepatocytes. In vivo and in vitro studies showed that Anthrax edema toxin (EdTx) induce lethal liver and heart damage We used microarrays to detail the global programme of gene expression underlying cellularisation and identified distinct classes of up-regulated and down-regulated genes during this process.
Project description:Human microvascular endothelial cells (HMVEC) treated with vascular endothelial growth factor (VEGF), Antrhax Edema Toxin (ET), or the Epac activator, 8-pCPT-2'-O-Me-cAMP (8CPT) Human microvascular endothelial cells (HMVEC) were treated with VEGF alone or VEGF in combination with either the the Epac-specific cAMP-mimetic, 8-pCPT-2'-O-Me-cAMP (8CPT), or anthrax edema toxin (ET), an adenylyl cyclase. ET or 8CPT can inhibit VEGF-mediated chemotaxis and angiogenesis. The goal of the study was to identify genes regulated by cAMP production (ET) or by activation of Epac/Rap (8CPT) that may mitigate the effects of VEGF treatment.
Project description:Human microvascular endothelial cells (HMVEC) treated with vascular endothelial growth factor (VEGF), Antrhax Edema Toxin (ET), or the Epac activator, 8-pCPT-2'-O-Me-cAMP (8CPT); Human microvascular endothelial cells (HMVEC) were treated with VEGF alone or VEGF in combination with either the the Epac-specific cAMP-mimetic, 8-pCPT-2'-O-Me-cAMP (8CPT), or anthrax edema toxin (ET), an adenylyl cyclase. ET or 8CPT can inhibit VEGF-mediated chemotaxis and angiogenesis. The goal of the study was to identify genes regulated by cAMP production (ET) or by activation of Epac/Rap (8CPT) that may mitigate the effects of VEGF treatment. Experiment Overall Design: Gene expression was measured 4 hours after treatment with VEGF, VEGF + 8CPT, VEGF + ET or mock treatment. Each sample contained one replicate.
Project description:Anthrax lethal toxin directly targets human peripheral monocytes and causes multiple aberrant gene responses that would be expected to result in defects in human monocyteM-bM-^@M-^Ys normal signaling transduction pathways and nction. This study provides further insights into the mechanisms associated with the host immune system collapse during an anthrax infection, and suggests that anthrax LT may have additional targets outside the well-known MAPK pathway. There were 4 replicates, 1 control and 1 toxin treated from 4 donors, with 8 samples total. key word : Toxin response
Project description:The activity of known anthrax lethal toxin is insufficient to account the effects on functions of cardiomyocytes. In vivo and in vitro studies showed that Anthrax lethal toxin (LeTx) induce heart damage We used microarrays to detail the global programme of gene expression underlying cellularisation and identified distinct classes of up-regulated and down-regulated genes during this process.
Project description:For tree crops, shortening juvenile phase is a vital strategy for early flowering that ensure to bear fruits in advance to enhance breeding efficiency. In walnut (Juglans regia L.), it usually takes 3-5 years for blooming, but the early flowering (EF) walnut can even flower in a year after planted. The juvenile phase of EF walnut is shorter than the late flowering (LF) walnut, which is more propitious to breeding efficiency. In this study, using RNA sequencing (RNA-seq) and microRNA-seq, we profiled transcriptome-wide identification of gene expression and microRNAs between EF and LF walnuts.