Analysis of gene expression changes in early mouse embryos lacking Tgif1 and Tgif2
Ontology highlight
ABSTRACT:
ORGANISM(S): Mus musculus
PROVIDER: GSE78728 | GEO | 2017/06/23
SECONDARY ACCESSION(S): PRJNA313327
REPOSITORIES: GEO
Similar Datasets
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. Primary MEFs were passaged on a 3T3 protocol and were harvested at passage 3 or 5, for RNA isolation and hybridization to Affymetrix microarrays.
2012-06-20 | E-GEOD-24225 | biostudies-arrayexpress
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
Project description:The aim of the study was to investigate the role of TGIF1 in MLL-AF9 transformed cells Members of the TALE (Three-amino acid loop extension) family of atypical homeodomain-containing transcription factors are prominent downstream effectors of oncogenic fusion proteins generated from translocations involving the mixed lineage leukemia (MLL) gene. A particular well-characterized member of this protein family is MEIS1, which together with HOXA proteins, orchestrates a transcriptional program required for the maintenance of MLL-rearranged acute myeloid leukemia (AML). Although TALE family proteins are mainly described as transcriptional activators TGIF1 (TGF-β induced factor) / TGIF2 are considered as transcriptional repressors. However, as their function in MLL-rearranged AML is largely unknown, we tested the potential importance of TGIF1 in the maintenance of MLL-rearranged AML. We find that expression of TGIF1 in MLL-AF9 transformed cells (MAF9) leads to cell cycle exit and differentiation in vitro and delayed leukemic onset in vivo. In accordance, MLL-rearranged patient blasts display lower levels of TGIF1 and TGIF1 expression in general correlates positively with survival. Mechanistically, we show that TGIF1 interferes with a MEIS1-dependent transcriptional program by associating to MEIS1-bound region in a competitive manner. Collectively, these findings demonstrate that TALE family members can act both positively and negatively on transcriptional programs responsible for the maintenance of MLL-rearranged AML.
2014-11-11 | GSE55713 | GEO
Project description:Members of the TALE (Three-amino acid loop extension) family of atypical homeodomain-containing transcription factors are prominent downstream effectors of oncogenic fusion proteins generated from translocations involving the mixed lineage leukemia (MLL) gene. A particular well-characterized member of this protein family is MEIS1, which together with HOXA proteins, orchestrates a transcriptional program required for the maintenance of MLL-rearranged acute myeloid leukemia (AML). Although TALE family proteins are mainly described as transcriptional activators TGIF1 (TGF-β induced factor) / TGIF2 are considered as transcriptional repressors. However, as their function in MLL-rearranged AML is largely unknown, we tested the potential importance of TGIF1 in the maintenance of MLL-rearranged AML. We find that expression of TGIF1 in MLL-AF9 transformed cells (MAF9) leads to cell cycle exit and differentiation in vitro and delayed leukemic onset in vivo. In accordance, MLL-rearranged patient blasts display lower levels of TGIF1 and TGIF1 expression in general correlates positively with survival. Mechanistically, we show that TGIF1 interferes with a MEIS1-dependent transcriptional program by associating to MEIS1-bound region in a competitive manner. Collectively, these findings demonstrate that TALE family members can act both positively and negatively on transcriptional programs responsible for the maintenance of MLL-rearranged AML.
2014-11-11 | GSE55287 | GEO
Project description:Colon tumors in mice were generated by deleting one allele of the Apc gene, or both alleles of Tgif1 and Tgif2, together with a single Apc allele. Gene expression was compared by RNA-seq analysis of wild type colon, Apc mutant tumors or Apc mutant colon tumors with deletion of both Tgif1 and Tgif2. Comparison of Apc tumors to Apc;Tgif1;Tgif2 tumors was used to identify Tgif-dependent gene expression changes associated with intestinal tumorigenesis.
2019-04-10 | GSE116578 | GEO
Project description:Eric Hesse 9 Jan 2019, 17:34 (15 hours ago) to me, Hartmut Lieber Marcel, unten ist das abstract kopiert, reicht das? Lg, Eric Abstract Osteoporosis is caused by increased bone resorption and decreased bone formation. Intermittent administration of a fragment of Parathyroid hormone (PTH) activates osteoblast-mediated bone formation and is used in patients with severe osteoporosis. However, the mechanisms by which PTH elicits its anabolic effect are not fully elucidated. Here we show that the absence of the homeodomain protein TG-interacting factor 1 (Tgif1) impairs osteoblast differentiation and activity, leading to a reduced bone formation. Deletion of Tgif1 in osteoblasts and osteocytes decreases bone resorption due to an increased secretion of Semaphorin 3E (Sema3E), an osteoclast-inhibiting factor. Tgif1 is a PTH target gene and PTH treatment failed to increase bone formation and bone mass in Tgif1-deficient mice. Thus, our study identifies Tgif1 as a novel regulator of bone remodeling and an essential component of the PTH anabolic action. These insights contribute to a better understanding of bone metabolism and the anabolic function of PTH.
2019-01-29 | PXD012303 | Pride
Project description:In this study we demonstrate that Tgif1 has a role in HSCs maintenance, self-renewal and quiescence. RNA sequencing data of LSK cells (HSCs enriched cell population) from Tgif1-/- and wild type mice implicates that multiple pathways involved in HSC quiescence and self-renewal are disturbed in Tgif1 deficient mice. RNA expression profiles of wild type (WT) and Tgif1-/- LSK cells were generated by RNA sequencing, in triplicate, using Illumina HiSeq 2000.
2013-09-10 | E-GEOD-50739 | biostudies-arrayexpress
Project description:In this study we demonstrate that Tgif1 has a role in HSCs maintenance, self-renewal and quiescence. RNA sequencing data of LSK cells (HSCs enriched cell population) from Tgif1-/- and wild type mice implicates that multiple pathways involved in HSC quiescence and self-renewal are disturbed in Tgif1 deficient mice.
2013-09-10 | GSE50739 | GEO
Project description:TG-interacting factor1 (Tgif1) is well-known as a transcriptional repressor in transforming growth factor beta (TGFβ) signaling pathway. Target mapping of ES core factors in mouse embryonic stem (ES) cells revealed that Tgif1 is occupied by Oct4 and Nanog. Moreover, recent interactome study of mouse gene regulatory regions showed a preferential regulation of Tgif1 by mouse ES cell specific enhancers. However, the detailed role and mode of actions of Tgif1 in stem cell maintenance and development remains elusive. We show that Tgif1 is indispensable for self-renewal and pluripotency of mouse embryonic stem (ES) cells. Aberrant expression of Tgif1 promotes differentiation of ES cells even in the presence of LIF in part by deregulation of pluripotency factors. Intriguingly, we find that Tgif1 level is a critical factor to determine specific lineage commitment in a dosage-dependent manner. We further show that Tgif1 interacts with ES cell core factors and co-localizes at their binding sites, which eventually restricts expression of ES cell core factors including Oct4, Sox2, and Nanog. Taken together, we provide new insights into the roles of Tgif1 in maintenance as well as differentiation of ES cells.
2015-09-26 | GSE55401 | GEO
Project description:TG-interacting factor1 (Tgif1) is well-known as a transcriptional repressor in transforming growth factor beta (TGFβ) signaling pathway. Target mapping of ES cell core factors in mouse embryonic stem (ES) cells revealed that Tgif1 is occupied by Oct4 and Nanog. Moreover, recent interactome study of mouse gene regulatory regions showed a preferential regulation of Tgif1 by mouse ES cell specific enhancers. However, the detailed role and mode of actions of Tgif1 in stem cell maintenance and development remains elusive. We show that Tgif1 is indispensable for self-renewal and pluripotency of mouse embryonic stem (ES) cells. Aberrant expression of Tgif1 promotes differentiation of ES cells even in the presence of LIF in part by deregulation of pluripotency factors. Intriguingly, we find that Tgif1 level is a critical factor to determine specific lineage commitment in a dosage-dependent manner. We further show that Tgif1 interacts with ES cell core factors and co-localizes at their binding sites, which eventually restricts expression of ES cell core factors including Oct4, Sox2, and Nanog. Taken together, we provide new insights into the roles of Tgif1 in maintenance as well as differentiation of ES cells.
2015-09-26 | GSE55404 | GEO