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Metabolomics,Unknown,Transcriptomics,Genomics,Proteomics

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Expression profiling of Aldh1l1-precursors in the developing spinal cord reveals glial lineage-specific genes and direct Sox9-Nfe2l1 interactions

ABSTRACT: Developmental regulation of gliogenesis in the mammalian CNS is incompletely understood, in part due to a limited repertoire of lineage-specific genes. We used Aldh1l1-GFP as a marker for gliogenic radial glia and later-stage precursors of developing astrocytes and performed gene expression profiling of these cells. We then used this dataset to identify candidate transcription factors that may serve as glial markers or regulators of glial fate. Our analysis generated a database of developmental stage-related markers of Aldh1l1+ cells between murine embryonic day 13.5-18.5. Using these data we identify the bZIP transcription factor Nfe2l1 and demonstrate that it promotes glial fate under direct Sox9 regulatory control. Thus, this dataset represents a resource for identifying novel regulators of glial development. 18 total samples consisting of three biological replicates each of flow sorted embryonic spinal cord Aldh1l1-GFP positive cells and whole cord, spanning the radial glial to astrocyte transition

ORGANISM(S): Mus musculus

SUBMITTER: David Rowitch

PROVIDER: E-GEOD-58614 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Expression profiling of Aldh1l1-precursors in the developing spinal cord reveals glial lineage-specific genes and direct Sox9-Nfe2l1 interactions

Project description:Developmental regulation of gliogenesis in the mammalian CNS is incompletely understood, in part due to a limited repertoire of lineage-specific genes. We used Aldh1l1-GFP as a marker for gliogenic radial glia and later-stage precursors of developing astrocytes and performed gene expression profiling of these cells. We then used this dataset to identify candidate transcription factors that may serve as glial markers or regulators of glial fate. Our analysis generated a database of developmental stage-related markers of Aldh1l1+ cells between murine embryonic day 13.5-18.5. Using these data we identify the bZIP transcription factor Nfe2l1 and demonstrate that it promotes glial fate under direct Sox9 regulatory control. Thus, this dataset represents a resource for identifying novel regulators of glial development.

2014-06-19 | GSE58614 | GEO

Transcription factor Achaete-Scute homologue 2 initiates T follicular helper cell development

Project description:This SuperSeries is composed of the SubSeries listed below. Refer to individual Series

2014-01-01 | E-GEOD-52840 | biostudies-arrayexpress

Transcription factor Achaete-Scute homologue 2 initiates T follicular helper cell development [array]

Project description:In immune responses, activated T cells migrate to B cell follicles and develop to T follicular helper (Tfh) cells, a new subset of CD4+ T cells specialized in providing help to B lymphocytes in the induction of germinal centers 1-3. Although Bcl6 has been shown to be essential in Tfh cell function, it may not regulate the initial migration of T cells 4 or the induction of Tfh program as exampled by CXCR5 upregulation 5. Here, we show that the Achaete-Scute homologue 2 (Ascl2) gene that encodes a basic helix-loop-helix (bHLH) transcription factor 6, is selectively upregulated in its expression in Tfh cells. Ectopic expression of Ascl2 uniquely upregulates CXCR5 but not Bcl6 and downregulates CCR7 expression in T cells in vitro and accelerates T cell migration to the follicles and Tfh cell development in vivo. Combined transcriptome profiling and genome-wide occupancy analysis indicate that Ascl2 directly regulates Tfh-related genes while inhibits expression of Th1 and Th17 genes. Acute deletion of Ascl2 as well as blockade of its function with the Id3 protein in peripheral CD4+ T cells results in a failure in Tfh cell development and the germinal center response. Conversely, mutation of Id3, known to cause antibody-mediated autoimmunity, greatly enhances Tfh cell generation. Thus, Ascl2 critically and directly initiates Tfh cell development. Decide gene expression patterns of CD4+ T cells with overexpressed Ascl2 or Tfh cells

2014-01-01 | E-GEOD-52838 | biostudies-arrayexpress

Microarray analysis of femoral artery injury in mice

Project description:To determine the differential expression of genes at sites of vascular injury in mice Four male, 5-6 mo old SMA-GFP mice (numbered 57, 60, 61, and 63) were subjected to fine wire femoral artery injury. The left femoral artery of each mouse was injured, and the contralateral artery was used as an uninjured control. The mice recovered from the injury procedure for 14 days, at which time they were sacrificed. The femoral arteries were removed and the adventitial side was extensively cleaned. The arteries were carefully opened longitudinally and immediately imaged for GFP. GFP-negative regions of the arteries, representing sites of vascular injury were microdissected, quick-frozen on dry ice, and stored in liquid nitrogen. Uninjured arteries were isolated and analyzed similarly; the entire uninjured artery was frozen. Total RNA was prepared. A 100-ng portion of each sample was subjected to linear amplification and hybridized to Affymetrix mouse gene 1.0ST.

2012-09-10 | E-GEOD-40637 | biostudies-arrayexpress

In Vivo Endothelial Cell Heterogeneity

Project description:Endothelial cells from nine steady state tissues and two regenerating tissues (bone marrow and liver) were intravitally labeld, isolated via flow sorting, and immediately processed for RNA extraction. When of sufficient quality, the RNA was amplified and hybridized. For comparison, Human Emybryonic Stem Cell-derived Endothelial cells (hESC-ECs) were differentiated and isolated based on similarities to the adult mouse counterparts. Endothelial cells were labeled via intravitally labeling of the vascular bed 8 minutes prior to sacrifice with minimally three markers to identify endothelial cells followed by flow sorting.

2013-07-15 | E-GEOD-47067 | biostudies-arrayexpress

Mechanosensitive proteins are sensitized in myelinated afferents following in vivo inflammation

Project description:Here we identified two populations of myelinated sensory neurons that display markedly different phenotypes in terms of their action potential characteristics and responses to mechanical stimuli based on their expression of Calcitonin Gene-Related Peptide (CGRP). Myelinated neurons that did not express CGRP responded to mechanical stimuli with significantly larger currents during whole-cell voltage clamp recordings than their CGRP-positive counterparts, regardless of whether these neurons projected to the dorsal hindpaw skin or the gastrocnemius muscle. Importantly, this discrepancy could not be explained by a differential expression of mechanosensitive or mechanically-gated proteins like Stoml3 or Piezo2. Following inflammation of the skin or muscle, myelinated neurons demonstrated a sensitization to mechanical stimuli characterized by increased current amplitudes. Interestingly, myelinated neurons expressing CGRP are sensitized to mechanical stimuli following cutaneous inflammation of the paw, while myelinated neurons that do not express CGRP are sensitized to mechanical stimuli following inflammation of the gastrocnemius muscle. Microarray data was obtained from these populations by first using Fluorescence-Activated Cell Sorting (FACS) to separate the populations of interest. 15 different samples were analyzed, 3 biological replicates for each group (5 groups: saline paw-injected, CFA paw-injected, saline muscle-injected, acid muscle-injected, and CFA muscle-injected). The saline injected groups (paw and muscle) are considered controls.

2015-11-06 | E-GEOD-65613 | biostudies-arrayexpress

Gene Array Analyzer (GAA): Alternative usage of gene arrays to study alternative splicing events (MoGene array)

Project description:The latest version of microarrays released by Affymetrix, the GeneChip Gene 1.0 ST Arrays (gene arrays), are designed in a similar fashion as exon arrays, which enables to identify differentially expressed exons, rather than only the expression level of whole transcripts. Here, we propose an extension, Gene Array Analyzer (GAA), to our previously published Exon Array Analyzer (EAA). GAA enables to analyse gene arrays on exon level and therefore supports to identify alternative splicing with gene arrays. To show the applicability of GAA, we used gene arrays to profile alternative splice events during the development of the heart. Further re-analysis of published gene arrays could show, that some of these splice events reoccur under pathological conditions. The web interface of GAA is user friendly, functional without set up and freely available at http://GAA.mpi-bn.mpg.de. Alternative splicing and gene expression analysis during development of the heart and cardiomyoyte differentiation.

2011-11-28 | E-GEOD-30429 | biostudies-arrayexpress

The histone demethylase Jarid1b ensures faithful mouse development by protecting developmental genes from aberrant H3K4me3

Project description:This SuperSeries is composed of the SubSeries listed below. Refer to individual Series

2013-04-26 | E-GEOD-41174 | biostudies-arrayexpress

The histone demethylase Jarid1b ensures faithful mouse development by protecting developmental genes from aberrant H3K4me3 [Affymetrix]

Project description:Embryonic development is tightly regulated by transcription factors and chromatin-associated proteins. H3K4me3 is associated with active transcription and H3K27me3 with gene repression, while the combination of both keeps genes required for development in a plastic state. Here we show that deletion of the H3K4me2/3 histone demethylase Jarid1b (Kdm5b/Plu1) results in major neonatal lethality due to respiratory failure. Jarid1b knockout embryos have several neural defects including disorganized cranial nerves, defects in eye development and increased incidences of exencephaly. Moreover, in line with an overlap of Jarid1b and Polycomb targets genes, Jarid1b knockout embryos display homeotic skeletal transformations typical for Polycomb mutants. Genome-wide analysis demonstrated that normally inactive genes encoding developmental regulators acquire aberrant H3K4me3 in early Jarid1b knockout embryos. H3K4me3 accumulates as embryonic development proceeds, leading to increased expression of neural master regulators in knockouts. Taken together, these results suggest that Jarid1b contributes to mouse development by protecting developmental genes from inappropriate acquisition of active histone modifications. * Lack of Jarid1b leads to major neonatal lethality and defects in neural systems * Jarid1b mutants display homeotic skeletal transformations * H3K4me3 is increased at inactive transcriptional regulators in Jarid1b-/- embryos * Chromatin changes are accompanied by elevated levels of key neural transcription factors RNA was extracted from heads of E8.5 embryos, three pools of 4 heads each were used per genotype

2013-04-26 | E-GEOD-41171 | biostudies-arrayexpress

p53 constrains progression to anaplastic thyroid carcinoma in a Braf-mutant mouse model of papillary thyroid cancer.

Project description:Anaplastic thyroid carcinoma (ATC) has among the worst prognosis of any solid malignancy. The low incidence of the disease has in part precluded systematic clinical trials and tissue collection, and there has been little progress in developing effective therapies. BRAF and TP53 mutations co-occur in a high proportion of ATC, particularly those associated with a precursor papillary thyroid carcinoma (PTC). In order to develop an adult-onset model of BRAF-mutant anaplastic thyroid carcinoma, we generated a novel thyroid-specific CreER transgenic mouse. We utilize a Cre-regulated BrafV600E mouse and a conditional Trp53 allelic series to demonstrate that p53 constrains progression from papillary to anaplastic thyroid carcinoma. Gene expression and immunohistochemical analyses of murine tumors identified the cardinal features of human ATC including loss of differentiation, local invasion, distant metastasis and rapid lethality. We employed small animal ultrasound imaging to monitor autochthonous tumors, and show that treatment with the selective BRAF inhibitor PLX4720 improved survival, but did not lead to tumor regression or suppress signaling through the MAPK pathway. Combination of PLX4720 and the MEK inhibitor PD0325901 more completely suppressed MAPK pathway activation in mouse and human ATC cell lines, and improved the structural response and survival of ATC-bearing animals. This model expands the limited repertoire of autochthonous models of clinically aggressive thyroid cancer, and these data suggest that small molecule MAPK pathway inhibitors hold clinical promise in the treatment of advanced thyroid carcinoma. Total RNA from five murine papillary thyroid carcinoma (PTC) tumors and five murine anaplastic thyroid carcinoma (ATC) tumors was analyzed.

2014-04-02 | E-GEOD-55933 | biostudies-arrayexpress

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