To characterize how symbiotic bacteria affect the lolecular and cellular mechanisms of epithelial homeostasis, human colonic Caco-2 cells
Epithelial cell proliferation arrest induced by lactate and acetate from Lactobacillus casei and Bifidobacterium breve.
No sample metadata fields
View SamplesIn order to identify the developmental changes controlling the switch from disease susceptibility to resistance, we performed global gene expression analysis on non-infected and infected intestinal tissues taken from 4-day- and 7-day-old animals.
Maturation of paneth cells induces the refractory state of newborn mice to Shigella infection.
Age
View Samplesto analyse the transcriptomic response of human intestinal tissue engrafted in SCID mice to Shigella infection
Virulent Shigella flexneri subverts the host innate immune response through manipulation of antimicrobial peptide gene expression.
No sample metadata fields
View SamplesPhosphorylation of histone H3 at Serine 10 emerges as a mechanism increasing chromatin accessibility of the transcription factor NF-kB for a particular set of immune genes. Here we report that a bacterial pathogen uses this strategy to shape the transcriptional response of infected host cells. We identify the Shigella flexneri type III protein effector OspF as a Dual Specific Phosphatase. OspF dephosphorylates MAP kinases within the nucleus impairing histone H3 phosphorylation at Serine 10 in a gene-specific manner. Therefore, OspF reprograms the transcriptional response for inactivation of a subset of NF-kB responsive genes. This regulation leads to repression of polymorphonuclear leukocytes recruitment in infected tissues. Thus, pathogens have evolved the ability to precisely modulate host cell epigenetic information as a strategy to repress innate immunity.
An injected bacterial effector targets chromatin access for transcription factor NF-kappaB to alter transcription of host genes involved in immune responses.
No sample metadata fields
View SamplesWe have here followed the transcriptional effect of stimulation with the phorbol ester PMA in mouse fibroblasts from HP1gamma null mice recomplemented with either wild-type HP1gamma or an HP1g with an S83A mutation Overall design: Spontaneously immortalized mouse embryonic fibroblasts from HP1gamma null mice were used to stably integrate either an empty expression vector, or expression vectors for either WT or S83A mutant HP1gamma. These cells were then stimulated with PMA for 0 or 60 min. and used for transcriptome analysis by Next Generation sequencing.
Shigella flexneri targets the HP1γ subcode through the phosphothreonine lyase OspF.
No sample metadata fields
View SamplesThe widespread use of wireless devices during the last decades is rising the concern about the adverse health effects of the radiofrequency electromagnetic radiation (RF-EMR) emitted from these devices. Studies are targeting on unrevealing the underlying mechanisms of RF-EMR action. The contribution of the omics high throughput approaches is a prerequisite towards this direction. In the present work, C57BL/6 adult male mice were sham-exposed (nSE=8) or whole-body exposed (nExp=8) for 2h to GSM 1800 MHz mobile phone radiation at 11 V/m average electric field intensity, and the RF-EMR effects on the hippocampal lipidome and transcriptome profile were evaluated. The data analysis of the phospholipids fatty acid residues revealed that the levels of six fatty acids (16:0, 16:1 6+7c, 18:1 9c, 20:5 w3, SFA, MUFA) were significantly altered (p<0.05) in the exposed group. The microarray data analysis demonstrated that the expression of 178 genes changed significantly (p<0.05) between the two groups with a fold change cut off of 1.5. In general, the observed changes point out the attention to a membrane remodeling response of the tissue phospholipids after non-ionizing radiation exposure, reducing the Saturated Fatty Acids (SFA) and EPA omega-3 (20:5 w3) and increasing Monounsaturated Fatty Acids (MUFA) residues and in parallel reflect an impact to genes implicated in critical biological processes, as cell cycle, DNA replication and repair, cell death, cell signaling, nervous system development and function, immune system response, lipid metabolism and cancer
Hippocampal lipidome and transcriptome profile alterations triggered by acute exposure of mice to GSM 1800 MHz mobile phone radiation: An exploratory study.
Specimen part
View SamplesBACKGROUND: p53 is an important tumor suppressor with a known role in the later stages of colorectal cancer, but its relevance to the early stages of neoplastic initiation remains somewhat unclear. Although p53-dependent regulation of Wnt signalling activity is known to occur, the importance of these regulatory mechanisms during the early stages of intestinal neoplasia has not been demonstrated.
A limited role for p53 in modulating the immediate phenotype of Apc loss in the intestine.
Specimen part
View SamplesThis SuperSeries is composed of the SubSeries listed below.
The long non-coding RNA Dali is an epigenetic regulator of neural differentiation.
Specimen part, Cell line
View SamplesMany intergenic long noncoding RNA (lncRNA) loci regulate the expression of adjacent protein coding genes. Less clear is whether intergenic lncRNAs commonly regulate transcription by modulating chromatin at genomically distant loci. Here, we report both genomically local and distal RNA-dependent roles of Dali, a conserved central nervous system expressed intergenic lncRNA. Dali is transcribed downstream of the Pou3f3 transcription factor gene and its depletion disrupts the differentiation of neuroblastoma cells. Locally, Dali transcript regulates transcription of the Pou3f3 locus. Distally, it preferentially targets active promoters and regulates expression of neural differentiation genes, in part through physical association with the POU3F3 protein. Dali interacts with the DNMT1 DNA methyltransferase in mouse and human and regulates DNA methylation status of CpG island-associated promoters in trans. These results demonstrate, for the first time, that a single intergenic lncRNA controls the activity and methylation of genomically distal regulatory elements to modulate large-scale transcriptional programmes.
The long non-coding RNA Dali is an epigenetic regulator of neural differentiation.
Specimen part, Cell line
View SamplesMany intergenic long noncoding RNA (lncRNA) loci regulate the expression of adjacent protein coding genes. Less clear is whether intergenic lncRNAs commonly regulate transcription by modulating chromatin at genomically distant loci. Here, we report both genomically local and distal RNA-dependent roles of Dali, a conserved central nervous system expressed intergenic lncRNA. Dali is transcribed downstream of the Pou3f3 transcription factor gene and its depletion disrupts the differentiation of neuroblastoma cells. Locally, Dali transcript regulates transcription of the Pou3f3 locus. Distally, it preferentially targets active promoters and regulates expression of neural differentiation genes, in part through physical association with the POU3F3 protein. Dali interacts with the DNMT1 DNA methyltransferase in mouse and human and regulates DNA methylation status of CpG island-associated promoters in trans. These results demonstrate, for the first time, that a single intergenic lncRNA controls the activity and methylation of genomically distal regulatory elements to modulate large-scale transcriptional programmes.
The long non-coding RNA Dali is an epigenetic regulator of neural differentiation.
Specimen part, Cell line
View Samples