Transcriptional profiling of tfap2a;tfap2c loss of function in zebrafish single whole embryos at 15 somites post fertilisation
Ontology highlight
ABSTRACT:
INSTRUMENT(S): Illumina HiSeq 2500
ORGANISM(S): Danio rerio
SUBMITTER: Christopher Dooley
PROVIDER: E-MTAB-6106 | biostudies-arrayexpress |
REPOSITORIES: biostudies-arrayexpress
Similar Datasets
Project description:Establish baseline expression transcriptional signatures for zebrafish developmental stages. Total RNA was extracted from single wild type zebrafish embryos at a series of different developmental stages. RNA from 12 embryos was pooled to generate a replicate.The RNA was DNase treated. Stranded RNAseq libraries were constructed using the Illumina TruSeq Stranded RNA protocol with oligo dT pulldown.This data is part of a pre-publication release. For information on the proper use of pre-publication data shared by the Wellcome Trust Sanger Institute (including details of any publication moratoria), please see http://www.sanger.ac.uk/datasharing/
2016-06-12 | E-ERAD-475 | biostudies-arrayexpress
Project description:This study is an attempt to characterize the molecular basis for the functional differences between TFAP2A and TFAP2C. Recent findings have highlighted a critical role for the TFAP2C (AP-2M-NM-3) transcription factor in maintaining the luminal phenotype through the regulation of luminal-associated genes. Of particular interest is that the highly homologous AP-2 family member, TFAP2A (AP-2M-NM-1), is expressed in luminal breast cancer but appears to have a functionally distinct role in gene regulation. There is 83% similarity between TFAP2A and TFAP2C with 76% identity in the carboxyl-half of the proteins containing the DNA binding and dimerization domains. Although the two family members appear to have complementary and overlapping roles in regulating neural crest development, they have clear functional differences with regard to regulation of ERM-NM-1 expression. The global genomic binding pattern for TFAP2A and TFAP2C is highly similar. Genomic binding for TFAP2A and TFAP2C in the regulatory region for luminal-associated genes further demonstrated co-localization of the two factors. On the other hand, clear functional differences exist when comparing the effect on the pattern of gene expression following knockdown of TFAP2A vs. TFAP2C. In each case, knockdown of TFAP2C resulted in an abrogation of expression (RNA and protein) of the luminal-associated gene, whereas, knockdown of TFAP2A had minimal or no effect. By contrast, a known TFAP2A target gene, CDKN1A, was responsive to TFAP2A only. 1 ChIP-Seq data for TFAP2A in human breast carcinoma cell line MCF-7. See associated publication.
2014-04-12 | E-GEOD-44257 | biostudies-arrayexpress
Project description:This study is an attempt to characterize the molecular basis for the functional differences between TFAP2A and TFAP2C. Recent findings have highlighted a critical role for the TFAP2C (AP-2γ) transcription factor in maintaining the luminal phenotype through the regulation of luminal-associated genes. Of particular interest is that the highly homologous AP-2 family member, TFAP2A (AP-2α), is expressed in luminal breast cancer but appears to have a functionally distinct role in gene regulation. There is 83% similarity between TFAP2A and TFAP2C with 76% identity in the carboxyl-half of the proteins containing the DNA binding and dimerization domains. Although the two family members appear to have complementary and overlapping roles in regulating neural crest development, they have clear functional differences with regard to regulation of ERα expression. The global genomic binding pattern for TFAP2A and TFAP2C is highly similar. Genomic binding for TFAP2A and TFAP2C in the regulatory region for luminal-associated genes further demonstrated co-localization of the two factors. On the other hand, clear functional differences exist when comparing the effect on the pattern of gene expression following knockdown of TFAP2A vs. TFAP2C. In each case, knockdown of TFAP2C resulted in an abrogation of expression (RNA and protein) of the luminal-associated gene, whereas, knockdown of TFAP2A had minimal or no effect. By contrast, a known TFAP2A target gene, CDKN1A, was responsive to TFAP2A only.
2014-04-12 | GSE44257 | GEO
Project description:We were interested in determining what genes might be controlled by TFAP2C and/or TFAP2A, either directly or indirectly through regulation of ER-alpha and potentially other signaling pathways. We performed an microarray analysis in MCF7 cells with elimination of either TFAP2C or TFAP2A. The patterns of gene expression with alteration of TFAP2 activity were compared to changes in expression induced by estrogen exposure. Knock-down of TFAP2C in the presence of estrogen altered the pattern of several known ERalpha-regulated genes and a number of genes outside the estrogen-regulated pathways. Experiment Overall Design: 6 samples were analyzed. Experiment Overall Design: 1. MCF7 cells treated with TFAP2C siRNA, without the presence of estrogen. Experiment Overall Design: 2.MCF7 cells treated with TFAP2C siRNA, with the presence of estrogen. Experiment Overall Design: 3.MCF7 cells treated with TFAP2A siRNA, without the presence of estrogen. Experiment Overall Design: 4.MCF7 cells treated with TFAP2A siRNA, with the presence of estrogen. Experiment Overall Design: 5.MCF7 cells with no siRNA treatment, without the presence of estrogen. Experiment Overall Design: 6.MCF7 cells with no siRNA treatment, with the presence of estrogen.
2008-06-16 | E-GEOD-8640 | biostudies-arrayexpress
Project description:We were interested in determining what genes might be controlled by TFAP2C and/or TFAP2A, either directly or indirectly through regulation of ER-alpha and potentially other signaling pathways. We performed an microarray analysis in MCF7 cells with elimination of either TFAP2C or TFAP2A. The patterns of gene expression with alteration of TFAP2 activity were compared to changes in expression induced by estrogen exposure. Knock-down of TFAP2C in the presence of estrogen altered the pattern of several known ERalpha-regulated genes and a number of genes outside the estrogen-regulated pathways. Keywords: Various siRNA treatments
2007-12-17 | GSE8640 | GEO
Project description:We have deleted TFAP2A and its redundantly-acting paralog TFAP2C in human melanoma SkMel28 cell lines and are assessing MITF binding using Cleavage Under Targets and Release Using Nuclease (CUT&RUN). Conversely, we deleted all copies of MITF in SkMEL28 cells and are similarly profiling TFAP2A bound loci. We predict TFAP2A functions as a pioneer factor for MITF during melanocyte development and that in the absence of TFAP2A, MITF binding at loci normally co-bound by MITF/TFAP2A will be disrupted.
2023-02-08 | GSE166359 | GEO
Project description:The complexity of gene regulation has created obstacles to defining mechanisms that establish the patterns of gene expression characteristic of the different clinical phenotypes of breast cancer. Transcription factor TFAP2C plays a critical role in the regulation of both estrogen receptor-alpha (ERM-NM-1) and c-ErbB2/HER2 (Her2). Herein, we performed chromatin immunoprecipitation and direct sequencing (ChIP-seq) for TFAP2C in four breast cancer cell lines representing different clinical phenotypes. Comparing the genomic binding sites for TFAP2C in the various cell lines, we identified that glutathione peroxidase (GPX1) is regulated by TFAP2C through an AP-2 regulatory region in the promoter of the GPX1 gene. Knock-down of TFAP2C, but not the related factor TFAP2A, resulted in an abrogation of GPX1 expression. Selenium-dependent GPX activity correlated with endogenous GPX1 expression, and overexpression of exogenous GPX1 induced GPX activity and significantly increased resistance to tert-butyl hydroperoxide. Methylation of the CpG island encompassing the AP-2 regulatory region was identified in cell lines where TFAP2C failed to bind the GPX1 promoter and GPX1 expression was unresponsive to TFAP2C. Furthermore, in cell lines where GPX1 promoter methylation was associated with gene silencing, treatment with 5-aza-dC (an inhibitor of DNA methylation) resulted in activation of GPX1 RNA and protein expression. Methylation of the GPX1 promoter was identified in approximately 20% of primary breast cancers and a highly significant correlation between TFAP2C and GPX1 expression was confirmed when considering only those tumors with an unmethylated promoter, whereas the related factor, TFAP2A, failed to demonstrate a correlation. The results demonstrate that TFAP2C regulates the expression of GPX1, which influences the redox state and sensitivity to oxidative stress induced by peroxides. Given the established role of GPX1 in breast cancer, the results provide an important mechanism for TFAP2C to further influence oncogenesis and progression of breast carcinoma cells. 4 ChIP-Seq data for TFAP2C in human breast carcinoma cell lines MCF-7, BT-474, MDA-MB-453 and SKBR-3.
2012-09-12 | E-GEOD-36351 | biostudies-arrayexpress
Project description:The complexity of gene regulation has created obstacles to defining mechanisms that establish the patterns of gene expression characteristic of the different clinical phenotypes of breast cancer. Transcription factor TFAP2C plays a critical role in the regulation of both estrogen receptor-alpha (ERα) and c-ErbB2/HER2 (Her2). Herein, we performed chromatin immunoprecipitation and direct sequencing (ChIP-seq) for TFAP2C in four breast cancer cell lines representing different clinical phenotypes. Comparing the genomic binding sites for TFAP2C in the various cell lines, we identified that glutathione peroxidase (GPX1) is regulated by TFAP2C through an AP-2 regulatory region in the promoter of the GPX1 gene. Knock-down of TFAP2C, but not the related factor TFAP2A, resulted in an abrogation of GPX1 expression. Selenium-dependent GPX activity correlated with endogenous GPX1 expression, and overexpression of exogenous GPX1 induced GPX activity and significantly increased resistance to tert-butyl hydroperoxide. Methylation of the CpG island encompassing the AP-2 regulatory region was identified in cell lines where TFAP2C failed to bind the GPX1 promoter and GPX1 expression was unresponsive to TFAP2C. Furthermore, in cell lines where GPX1 promoter methylation was associated with gene silencing, treatment with 5-aza-dC (an inhibitor of DNA methylation) resulted in activation of GPX1 RNA and protein expression. Methylation of the GPX1 promoter was identified in approximately 20% of primary breast cancers and a highly significant correlation between TFAP2C and GPX1 expression was confirmed when considering only those tumors with an unmethylated promoter, whereas the related factor, TFAP2A, failed to demonstrate a correlation. The results demonstrate that TFAP2C regulates the expression of GPX1, which influences the redox state and sensitivity to oxidative stress induced by peroxides. Given the established role of GPX1 in breast cancer, the results provide an important mechanism for TFAP2C to further influence oncogenesis and progression of breast carcinoma cells.
2012-09-12 | GSE36351 | GEO
Project description:In order to establish a consensus catalog of dorsal rott ganglion cell types, we used comprehensive transcriptome analysis of single cells for unsupervised identification and molecular classification of sensory neurons independent of any a priori knowledge of sensory subtypes. RNA-Seq was performed on 799 dissociated single cells dissected from the mouse lumbar dorsal root ganglion distributed over a total of nine 96-well plates
2014-11-24 | E-GEOD-59739 | biostudies-arrayexpress
Project description:To elucidate the molecular basis of BMP4-induced differentiation of human pluripotent stem cells (PSCs) toward progeny with trophectoderm characteristics, we produced transcriptome, epigenome H3K4me3, H3K27me3, and CpG methylation maps of trophoblast progenitors, purified using the surface marker APA. We combined them with the temporally resolved transcriptome of the preprogenitor phase and of single APA+ cells. This revealed a circuit of bivalent TFAP2A, TFAP2C, GATA2, and GATA3 transcription factors, coined collectively the “trophectoderm four” (TEtra), which are also present in human trophectoderm in vivo. At the onset of differentiation, the TEtra factors occupy multiple sites in epigenetically inactive placental genes and in OCT4. Functional manipulation of GATA3 and TFAP2A indicated that they directly couple trophoblast-specific gene induction with suppression of pluripotency. In accordance, knocking down GATA3 in primate embryos resulted in a failure to form trophectoderm. The discovery of the TEtra circuit indicates how trophectoderm commitment is regulated in human embryogenesis.
2017-10-26 | GSE105022 | GEO