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Expression analysis of mouse embryo fibrobalsts lacking Tgif1

ABSTRACT: Tgif1 is a transcriptional corepressor that limits TGFβ responsive gene expression. TGFβ signaling has antiproliferative effects in several cell types, generally resulting in a G1 arrest. Mouse embryo fibroblasts (MEFs) are primary cells with limited life-span, that senesce after several passages in culture. We compared expression profiles of primary MEFs lacking Tgif1 with wild types at passage three, and with wild type MEFs at passage 5, to identify changes in gene expression due to loss of Tgif1 and due to increasing passage number. Primary MEFs were passaged on a 3T3 protocol and were harvested at passage 3 or 5, for RNA isolation and hybridization to Affymetrix microarrays.

ORGANISM(S): Mus musculus

SUBMITTER: David Wotton

PROVIDER: E-GEOD-24225 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Premature senescence and increased TGFβ signaling in the absence of Tgif1.

Zerlanko Brad J BJ Bartholin Laurent L Melhuish Tiffany A TA Wotton David D

PloS one 20120413 4

Transforming growth factor β (TGFβ) signaling regulates cell cycle progression in several cell types, primarily by inducing a G1 cell cycle arrest. Tgif1 is a transcriptional corepressor that limits TGFβ responsive gene expression. Here we demonstrate that primary mouse embryo fibroblasts (MEFs) lacking Tgif1 proliferate slowly, accumulate increased levels of DNA damage, and senesce prematurely. We also provide evidence that the effects of loss of Tgif1 on proliferation and senescence are not li ...[more]

PMID: 22514746

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Expression analysis of mouse embryo fibrobalsts lacking Tgif1

Project description:Tgif1 is a transcriptional corepressor that limits TGFβ responsive gene expression. TGFβ signaling has antiproliferative effects in several cell types, generally resulting in a G1 arrest. Mouse embryo fibroblasts (MEFs) are primary cells with limited life-span, that senesce after several passages in culture. We compared expression profiles of primary MEFs lacking Tgif1 with wild types at passage three, and with wild type MEFs at passage 5, to identify changes in gene expression due to loss of Tgif1 and due to increasing passage number.

2012-06-21 | GSE24225 | GEO

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2010-03-06 | E-GEOD-15325 | biostudies-arrayexpress

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Proteomic and phosphoproteomic profiling of mouse embryonic fibroblasts

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Transcription profiling of mouse embryonic fibroblasts from HtrA2 knockoutafter rotenone treatment. HtrA2 knockout mice have a movement disorder which may be similar to Parkinsons disease

Project description:Cellular stress responses can be activated following functional defects in organelles such as mitochondria and the endoplasmic reticulum. Mitochondrial dysfunction caused by loss of the serine protease HtrA2 leads to a progressive movement disorder in mice and has been linked to parkinsonian neurodegeneration in humans. Here we demonstrate that loss of HtrA2 results in transcriptional up-regulation of nuclear genes characteristic of the integrated stress response, including the transcription factor CHOP, selectively in the brain. We also show that loss of HtrA2 results in the accumulation of unfolded proteins in the mitochondria, defective mitochondrial respiration and enhanced production of reactive oxygen species that contribute to the induction of CHOP expression and to neuronal cell death. CHOP expression is also significantly increased in Parkinsonâs disease patientsâ brain tissue. We therefore propose that this brain-specific transcriptional response to stress may be important in the advance of neurodegenerative diseases. Experiment Overall Design: This experiment was set out to identify genes that are differentially regulated upon rotenone treatment in HtrA2 knockout (KO) mouse embryonic fibroblasts (MEFs) compared to wild type (WT) MEFs. Primary MEFs were isolated and at passage 4 subjected to treatment with vehicle (control) or 1 Î¼M rotenone (rot) for 4 hrs. 3 replicates were performed. RNA was isolated and samples were processed for hybridisation (12 samples in total).

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