Metabolomics,Unknown,Transcriptomics,Genomics,Proteomics

Dataset Information

Retinoic acid (RA) induction time-course to profile gene expression during mES cell differentiation

ABSTRACT: Murine ES cell gene expression before RA induction are used to compare gene expression for time-points of 8, 12, 16, 24, 36, 48, 60 and 72 hours post-induction. KH2 ES Cell RA Differentiation Time-course

ORGANISM(S): Mus musculus

SUBMITTER: Jeff Johnston

PROVIDER: E-GEOD-34279 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Publications

Poised RNA polymerase II changes over developmental time and prepares genes for future expression.

Gaertner Bjoern B Johnston Jeff J Chen Kai K Wallaschek Nina N Paulson Ariel A Garruss Alexander S AS Gaudenz Karin K De Kumar Bony B Krumlauf Robb R Zeitlinger Julia J

Cell reports 20121220 6

Poised RNA polymerase II (Pol II) is predominantly found at developmental control genes and is thought to allow their rapid and synchronous induction in response to extracellular signals. How the recruitment of poised RNA Pol II is regulated during development is not known. By isolating muscle tissue from Drosophila embryos at five stages of differentiation, we show that the recruitment of poised Pol II occurs at many genes de novo and this makes them permissive for future gene expression. A com ...[more]

PMID: 23260668

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Project description:Pentavalent vanadium compounds induce intracellular changes in vitro that are consistent with those of other carcinogenic substances, including alteration of transcription factor levels, promotion of oxidative stress, inflammation, DNA damage, stimulation of mitogenic signals, and suppression of apoptosis. While there is no clear evidence that vanadium compounds cause cancer in humans, vanadium pentoxide causes lung cancer in rodents after long-term inhalation exposures and in turn IARC has categorized it as a group 2B possible human carcinogen. The goal of this study was to investigate the carcinogenicity of NaVO3 in the human immortalized bronchial epithelial cell line, Beas-2B. Cells were treated with 10 ÂµM NaVO3 for 5 weeks, with or without recovery time, followed by gene expression microarray analysis. In a separate experiment, cells were exposed to 1-10 ÂµM NaVO3 for 4 weeks and then grown in soft agar to test for anchorage-independent growth. A dose-dependent increase in the number of colonies was observed. NaVO3-transformed clones could repair a wound faster than controls during the scratch test. In a gene expression microarray analysis of soft agar clones there were 2010 differentially expressed genes (DEG) (adjusted p-value â¤ 0.05) in NaVO3-transformed clones relative to control clones. DEG from this experiment were compared with the DEG of 5 week NaVO3 exposure with or without recovery, all with adjusted p-values <0.05, and 469 genes were altered in the same direction for transformed clones, 5 week NaVO3-treated cells, and the recovered cells; a subset of these changes were validated by QRT-PCR. The data from this study imply that chronic exposure to NaVO3 causes changes that are consistent with cellular transformation including anchorage- independent growth, enhanced migration ability, and gene expression changes that were epigenetically inherited through cell division. Beas-2B cells were chronically exposed to sodium metavanadate in growth media for 4 weeks. Then exposed cells and unexposed control cells were grown in soft agar for 3 weeks in the absence of vanadate. Transformed colonies (arising from vanadate-exposed cells) and control colonies (spontaneously grew from unexposed cells) were extracted from soft agar and expanded in the absence of vanadate, then processed for gene expression analysis on Affymetrix GeneChip Human Exon 1.0 ST array. 5 transformed clones, 3 control clones, 1 parental Beas-2B cell sample, and acute 24 hour vanadate exposed cell samples were analyzed.

Project description:Pentavalent vanadium compounds induce intracellular changes in vitro that are consistent with those of other carcinogenic substances, including alteration of transcription factor levels, promotion of oxidative stress, inflammation, DNA damage, stimulation of mitogenic signals, and suppression of apoptosis. While there is no clear evidence that vanadium compounds cause cancer in humans, vanadium pentoxide causes lung cancer in rodents after long-term inhalation exposures and in turn IARC has categorized it as a group 2B possible human carcinogen. The goal of this study was to investigate the carcinogenicity of NaVO3 in the human immortalized bronchial epithelial cell line, Beas-2B. Cells were treated with 10 M-BM-5M NaVO3 for 5 weeks, with or without recovery time, followed by gene expression microarray analysis. In a separate experiment, cells were exposed to 1-10 M-BM-5M NaVO3 for 4 weeks and then grown in soft agar to test for anchorage-independent growth. A dose-dependent increase in the number of colonies was observed. NaVO3-transformed clones could repair a wound faster than controls during the scratch test. In a gene expression microarray analysis of soft agar clones there were 2010 differentially expressed genes (DEG) (adjusted p-value M-bM-^IM-$ 0.05) in NaVO3-transformed clones relative to control clones. DEG from this experiment were compared with the DEG of 5 week NaVO3 exposure with or without recovery, all with adjusted p-values <0.05, and 469 genes were altered in the same direction for transformed clones, 5 week NaVO3-treated cells, and the recovered cells; a subset of these changes were validated by QRT-PCR. The data from this study imply that chronic exposure to NaVO3 causes changes that are consistent with cellular transformation including anchorage- independent growth, enhanced migration ability, and gene expression changes that were epigenetically inherited through cell division. Beas-2B cells were chronically exposed to sodium metavanadate in growth media for 4 weeks. Then, one set of exposed cells and unexposed control cells were grown in soft agar for 3 weeks in the absence of vanadate. Transformed colonies (arising from vanadate-exposed cells) and control colonies (spontaneously grew from unexposed cells) were extracted from soft agar and expanded in the absence of vanadate, then processed for gene expression analysis . A second set of exposed cells continued treatment for a total of 5 weeks exposure. A third set of cells recovered for 1 week after the 4 week long exposure. The gene expression of 5 transformed clones, 3 control clones, 2 5 week exposures, 2 recovery, and 2 unexposed control cells, and 1 parental Beas-2B cell samples were analyzed (15 total samples) with an Affymetrix GeneChip Human Exon 1.0 ST array.

Dataset Information

Retinoic acid (RA) induction time-course to profile gene expression during mES cell differentiation

Publications

Poised RNA polymerase II changes over developmental time and prepares genes for future expression.

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