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Expression data from mouse perigonadal white adipose tissue - various mutant conditions [gene-level analysis]

ABSTRACT: Progerin-expressing mice (HGPS-like) demonstrated increased energy metabolism and lipodystrophy. Increased mitochondrial biogenesis was found in adipose tissue from HGPS-like mice, whereas lamin C-only mice had fewer mitochondria. Thus we analyse which molecular pathways mediated the changes in adipose tissue caused by lamin C and progerin expression and the roles of these pathways in energy metabolism and aging. 10 cDNAs samples were analysed. We compared the mean fold change of 2 to 4 biological replicates. We performed an unpaired Student’s t-test to compare intensities in the different biological replicates. Genes were considered significantly regulated when the fold change was ≥ 1.5, and the p-value was ≤0.05.

ORGANISM(S): Mus musculus

SUBMITTER: Pierre de la Grange

PROVIDER: E-GEOD-51202 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Antagonistic functions of LMNA isoforms in energy expenditure and lifespan.

Lopez-Mejia Isabel C IC de Toledo Marion M Chavey Carine C Lapasset Laure L Cavelier Patricia P Lopez-Herrera Celia C Chebli Karim K Fort Philippe P Beranger Guillaume G Fajas Lluis L Amri Ez Z EZ Casas Francois F Tazi Jamal J

EMBO reports 20140317 5

Alternative RNA processing of LMNA pre-mRNA produces three main protein isoforms, that is, lamin A, progerin, and lamin C. De novo mutations that favor the expression of progerin over lamin A lead to Hutchinson-Gilford progeria syndrome (HGPS), providing support for the involvement of LMNA processing in pathological aging. Lamin C expression is mutually exclusive with the splicing of lamin A and progerin isoforms and occurs by alternative polyadenylation. Here, we investigate the function of lam ...[more]

PMID: 24639560

Similar Datasets

Expression data from mouse perigonadal white adipose tissue - various mutant conditions [exon-level analysis]

Project description:Progerin-expressing mice (HGPS-like) demonstrated increased energy metabolism and lipodystrophy. Increased mitochondrial biogenesis was found in adipose tissue from HGPS-like mice, whereas lamin C-only mice had fewer mitochondria. Thus we analyse which molecular pathways mediated the changes in adipose tissue caused by lamin C and progerin expression and the roles of these pathways in energy metabolism and aging. 10 cDNAs samples were analysed. We compared the mean fold change of 2 to 4 biological replicates. We performed an unpaired Student’s t-test to compare intensities in the different biological replicates. Genes were considered significantly regulated when the fold change was ? 1.5, and the p-value was ?0.05.

2015-06-05 | E-GEOD-51203 | biostudies-arrayexpress

Expression data from mouse perigonadal white adipose tissue - various mutant conditions

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

2015-06-05 | E-GEOD-51204 | biostudies-arrayexpress

ABT-737 treatment induces regulation and activation of pathways implicated in cell survival, proliferation and stem cells in treated AML mice survival, proliferation and stem cells in treated AML mice

Project description:Myelodysplastic syndrome (MDS) transforms into an acute myelogenous leukemia (AML) with associated increased bone marrow blast infiltration. Using a transgenic mouse model, MRP8[NRASD12/hBCL-2], in which the NRAS:BCL-2 complex at the mitochondria induces MDS progressing to AML with dysplastic features, we studied the therapeutic potential of a BCL-2 homology domain 3 (BH3) mimetic inhibitor, ABT-737. Treatment significantly extended lifespan, increased survival of lethally irradiated secondary recipients transplanted with treated cells compared with cells from untreated mice, with a reduction of bone marrow (BM) blasts, LSK and progenitor populations by increased apoptosis of infiltrating blasts of diseased mice assessed in vivo by Tc-99m-labeled Annexin V single photon emission computed tomography (SPECT) and ex vivo by Annexin V/7AAD flow cytometry, TUNEL, caspase 3 cleavage and re-localization of the NRAS:BCL-2 complex from mitochondria to plasma membrane. Phosphoprotein analysis showed restoration of wild-type AKT, ERK1/2 and MEK patterns in spleen cells after treatment, which show reduced mitochondrial membrane potential. Exon specific gene expression profiling corroborates the reduction of leukemic cells, with an increase in expression of genes coding for stem cell development and maintenance, myeloid differentiation and apoptosis. Myelodysplastic features persist underscoring targeting of BCL-2-mediated effects on MDS-AML transformation and survival of leukemic cells. NRASD12/BCL-2 double transgenic mice were analysed by enriching for primitive Sca1+ cells from splenocytes from untreated and ABT-737 treated mice. RNA was extracted analysed for gene expression profiles using exon specific arrays.

2013-11-06 | E-GEOD-48601 | biostudies-arrayexpress

Argonaute proteins couple chromatin silencing to alternative splicing (exon array)

Project description:While Argonaute (AGO) proteins play a major role in transcriptional gene silencing (TGS) in many organisms, their role in the nucleus of somatic mammalian cells remains elusive. Here, we have purified AGO1 and AGO2 chromatin-embedded complexes, and found these proteins associated with previously described partners, but also with chromatin modifiers and, rather unexpectedly, with different splicing factors. Using the CD44 gene as a model for alternative splicing, we show that both AGO1 and AGO2 are required for Protein Kinase C (PKC)-dependent variant exon inclusion. AGO proteins facilitate the spliceosome recruitment and modulate the elongation rate of RNA polymerase II (RNAPII). The recruitment of AGO proteins to CD44 transcribed region is dependent on both the endonuclease Dicer and the chromodomain-containing protein HP1g, and results in locally increased levels of histone H3 lysine 9 (H3K9) methylation on variant exons. Genome wide analysis of splicing in either AGO2 or Dicer null cells showed that the two proteins have similar effects on many splicing events. Finally, sRNAs associated with nuclear AGO2 are mostly in sense orientation relative to protein-coding genes, supporting a role for intragenic antisense non-coding RNAs in the recruitment AGO and splicing factors. Together, our data demonstrate for the first time that the endogenous RNAi pathway is involved in alternative splicing decisions, unravelling a new model in which AGO proteins couple RNAPII elongation and chromatin modification. Study of AGO2 or Dicer knock-out on gene expression and splicing regulation in MEF cells Transcriptome analysis of AGO2 and Dicer null MEF cells on GeneChipM-BM-. Mouse Exon 1.0 ST Arrays (Affymetrix). Dicer null MEF cells and wild-type MEF cells were from M. Otsuka. AGO2 null MEF cells were from A. Tarakhovsky. Experiment has been done in experimental triplicates. 9 Total samples were analyzed.

2012-09-10 | E-GEOD-39746 | biostudies-arrayexpress

Identification of the altered transcripts in the NMF291–/– cerebellum by exon array.

Project description:The U2 snRNA is a basal component of the major spliceosome, which is responsible for >90% human pre-mRNA splicing. A 5-nucleotide deletion in one of the mouse U2 snRNA genes (Rnu2-8) causes cerebellar granule cell degeneration in the NMF291 mouse mutant strain. To identify the altered transcripts in the NMF291–/– cerebellum, we interograted Affy. mouse 1.0 ST Exon arrays with total RNAs from three postnatal-30-day (P30) wild type and three NMF291–/– cerebella. Affy. mouse 1.0 ST Exon arrays were hybridized with total RNAs derived from three P30 female wild type and NMF291–/– mice (biological replicates).

2011-10-19 | E-GEOD-33069 | biostudies-arrayexpress

The data of differentially regulated exons from mouse testes - wild-type and Dazap1 mutant

Project description:The binding of Deleted in Azoospermia Associated Protein 1 (DAZAP1) to splicing mutations in the BRCA1 and NF1 genes that caused exon exclusion suggest a role for DAZAP1 in RNA splicing. To elucidate the biological functions of DAZAP1 and to search for its natural RNA substrates, we compared the exon usages of wild-type and Dazap1 mutant testes by exon microarrays. We used wild-type and Dazap1 mutant mouse testes. Each genotype has three replicates. 6 total samples were analyzed.

2013-06-01 | E-GEOD-42603 | biostudies-arrayexpress

The effect of progerin expression on alternative splicing in keratinocytes of HGPS mice

Project description:Exon level expression analysis for the HGPS pathological aging study data set to analyze the effect of progerin expression on alternative splicing in keratinocytes of HGPS mice. Analysis of the effect of pathological aging (transgenic progerin expression) on alternative splicing (AS) using exon microarrays to interrogate the differential exon usage of the entire genome of HGPS mice (postnatal day 24 and 35) and their wild-type litter mates. Our results suggests that early expression of progerin impairs developmental splicing but that as progerin accumulates, the number of genes with AS increases, similar to what is observed in aging wild-type mice. This dataset is one of the 2 datasets in the overall study. An additional data set series is available with exon expression analysis of aging wild-type mice to analyze the effect of age on alternative splicing during physiological aging. The two datasets are linked together in the SuperSeries GSE67289. A link to the SuperSeries is available at the bottom of this page. 16 skin keratinocyte samples from 2 different age groups: postnatal day 24 and postnatal day 35, from 8 HGPS samples and 8 genotype negative (wild-type) littermates.

2015-11-01 | E-GEOD-67288 | biostudies-arrayexpress

Differentially regulated exons from wild-type and Dazap1 mutant mouse testes

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

2013-06-01 | E-GEOD-42604 | biostudies-arrayexpress

Effect of progerin on p53-deficient vascular smooth muscle cells

Project description:Analysis of p53-deficient (E6-expressing) human vascular smooth muscle cells (VSMCs) that express progerin, a mutated form of lamin A resposible for Hutchinson- Gilford progeria syndrome (HGPS). p53 pathway is associated with HGPS. Results provide insight into molecular mechanisms underlying vascular dysfunction of HGPS caused by other than p53 pathway. The gene expression of VSMCs induced to express E6 and either lamin A or progerin by retroviral vectors.

2013-09-22 | E-GEOD-47553 | biostudies-arrayexpress

Argonaute proteins couple chromatin silencing to alternative splicing

Project description:This SuperSeries is composed of the following subset Series: GSE39746: Argonaute proteins couple chromatin silencing to alternative splicing (exon array) GSE39748: Argonaute proteins couple chromatin silencing to alternative splicing (RNA IP-Seq) Refer to individual Series

2012-08-22 | E-GEOD-39749 | biostudies-arrayexpress

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