Tfap2a dependnt cha
Ontology highlight
ABSTRACT:
ORGANISM(S): Mus musculus
PROVIDER: GSE60058 | GEO | 2014/08/05
SECONDARY ACCESSION(S): PRJNA257398
REPOSITORIES: GEO
Similar Datasets
Project description:Neo/null loss of Tfap2a in E10.5 mouse facial prominences triplicate run comparing tissue dissected from the nasal, maxillary and mandibular comparing AP-2 mutant and control embryos
2014-08-05 | E-GEOD-60058 | biostudies-arrayexpress
Project description:To investigate the role of the transcription factor AP-2 in craniofacial development, we performed: ATAC-seq on E11.5 craniofacial surface ectoderm in control and Tfap2a/Tfap2b ectoderm knock-out embryos; RNA-seq on E10.5 craniofacial prominences from control and Tfap2a/Tfap2b ectoderm knock-out embryos; histone-seq (H3K4me3) in E10.5 and E11.5 wild-type craniofacial surface ectoderm.
2022-03-28 | GSE199341 | GEO
Project description:To investigate the role of the transcription factor AP-2 in craniofacial development, we performed: ATAC-seq on E11.5 craniofacial surface ectoderm in control and Tfap2a/Tfap2b ectoderm knock-out embryos; RNA-seq on E10.5 craniofacial prominences from control and Tfap2a/Tfap2b ectoderm knock-out embryos; histone-seq (H3K4me3) in E10.5 and E11.5 wild-type craniofacial surface ectoderm.
2022-03-28 | GSE199340 | GEO
Project description:To investigate the role of the transcription factor AP-2 in craniofacial development, we performed: ATAC-seq on E11.5 craniofacial surface ectoderm in control and Tfap2a/Tfap2b ectoderm knock-out embryos; RNA-seq on E10.5 craniofacial prominences from control and Tfap2a/Tfap2b ectoderm knock-out embryos; histone-seq (H3K4me3) in E10.5 and E11.5 wild-type craniofacial surface ectoderm.
2022-03-28 | GSE199339 | GEO
Project description:Growth and patterning of the face relies on several small buds of tissue, the facial prominences, which surround the primitive mouth. Beginning around E10 of mouse development the prominences undergo rapid growth and morphogenesis. By E11.5 the medial nasal prominences are in close apposition in the midline, as are the maxillary and medial nasal prominences on either side of the developing face. Subsequently, by E12.5 the nasal and maxillary prominences fuse to form a continuous shelf at the front of the face - the primary palate. Individual prominences are associated with specific developmental processes, and this is reflected by patterns of differential gene expression that give the prominences their unique identities. Thus, only the mandibular and maxillary prominences give rise to dentition while the frontonasal prominence has a unique role in olfaction, and the mandibular prominence in taste. We used microarrays to detail the differential gene expression program in each of the mandibular, maxillary, and frontonasal prominences during the key developmental timepoints of E10.0 through E12.5. Experiment Overall Design: Analysis of gene expression during growth and fusion of the facial prominences in the C57BL/6J mouse strain between embryonic (E) day 10.0 and 12.5. At the earliest timepoint, E10, only the mandibular prominence is a distinct entity that can be readily identified and dissected. The frontonasal prominence and the maxillary prominence are very small and not discrete from other components of the head such as the forebrain until E10.5. Analysis of these tissues at earlier timepoints would require laser capture and preamplification steps - techniques that were not used for the later timepoints. Thus samples were isolated from the mandibular prominence at E10.0 and from the mandibular, maxillary and frontonasal prominences of mouse embryos from E10.5 to E12.5, at 0.5 day intervals. In order to obtain sufficient sample for hybridization, each sample represents a pool of between 3 and 48 embryos depending on the timepoint. Specifically, the number of embryos were 40-48 for E10.0 (mandibular prominence only), 24-8 for E10.5, 8-9 for E11.0 and E11.5 and 3-4 for E12.0 and E12.5. Seven replicate samples were taken for each of the later five timepoints in each of the three prominences, with an additional seven samples for the mandibular E10.0 timepoint, for a total of 112 samples.
2008-10-26 | E-GEOD-7759 | biostudies-arrayexpress
Project description:We present a gene expression atlas of early mouse craniofacial development. Laser capture microdissection (LCM) was used to isolate cells from the principal critical micro-regions, whose development, differentiation and signaling interactions are responsible for the construction of the mammalian face We examined the facial mesenchyme and adjacent neuroepithelium at E8.5, at E9.5 we obtain cells from the facial mesenchyme, olfactory placode/epidermal ectoderm, underlying neuroepithileium, and emerging mandibular and maxillary arches. AT E10.5 we sampled the medial and lateral prominences, olfactory pit, multiple regions of the underlying neuroepithelium the mandibular and maxillary arches, and Rathke's pouch. Mouse emrbyos were harvested at developmental stage E8.5 , E9.5, and E10.5 and cells were captured from microregions responsible for the construction of the mammalian face. RNA was extracted, labelled, and quantified using the Mouse ST-l microarray.
2014-03-18 | E-GEOD-55965 | biostudies-arrayexpress
Project description:This investigation provides a robust multi-dimensional compendium of gene expression data relevant to mouse facial development. It profiles the transcriptome ofectoderm and mesenchyme from the three facial prominences in a time series encompassing their growth and fusion. Analysis of the dataset identified more than 8000 differentially expressed genes comprising dramatically different ectoderm and mesenchyme programs. The mesenchyme programs included many genes identified in earlier analyses as well hundreds of genes not previously implicated in craniofacial development. The ectoderm programs included over a thousand genes that highlight epithelial structure, cell-cell interactions and signaling. The dataset includes 45 .cel files, DABG probability and RMA log2 expression values for each probeset, and statistics for 9457 probesets representing 8575 genes. 45 total samples, with 15 conditions sampling three ages (E10.5, E11.5, E12.5), three facial prominences (mandibular, maxillary and fronto-nasal) and two tissue layers (ectoderm or mesenchyme), with 3 biological replicates per condition. Differential expression was determined after median filter for variance with three-way ANOVA, Benjamini-Hochberg multiple testing correction
2014-10-10 | E-GEOD-62214 | biostudies-arrayexpress
Project description:Mutations in the gene encoding transcription factor TFAP2A result in pigmentation anomalies in model organisms and premature hair graying in humans. However, the pleiotropic functions of TFAP2A and its redundantly-acting paralogs have made the precise contribution of TFAP2-type activity to melanocyte differentiation unclear. Defining this contribution may help to explain why TFAP2A expression is reduced in advanced-stage melanoma compared to benign nevi. To identify genes with TFAP2A-dependent expression in melanocytes, we profile zebrafish tissue and mouse melanocytes deficient in Tfap2a, and find that expression of a small subset of genes underlying pigmentation phenotypes is TFAP2A-dependent, including Dct, Mc1r, Mlph, and Pmel. We then conduct TFAP2A ChIP-seq in mouse and human melanocytes and find that a much larger subset of pigmentation genes is associated with active regulatory elements bound by TFAP2A. These elements are also frequently bound by MITF, which is considered the “master regulator” of melanocyte development. For example, the promoter of TRPM1 is bound by both TFAP2A and MITF, and we show that the activity of a minimal TRPM1 promoter is lost upon deletion of the TFAP2A binding sites. However, the expression of Trpm1 is not TFAP2A-dependent, implying that additional TFAP2 paralogs function redundantly to drive melanocyte differentiation, which is consistent with previous results from zebrafish. Paralogs Tfap2a and Tfap2b are both expressed in mouse melanocytes, and we show that mouse embryos with Wnt1-Cre-mediated deletion of Tfap2a and Tfap2b in the neural crest almost completely lack melanocytes but retain neural crest-derived sensory ganglia. These results suggest that TFAP2 paralogs, like MITF, are also necessary for induction of the melanocyte lineage. Finally, we observe a genetic interaction between tfap2a and mitfa in zebrafish, but find that artificially elevating expression of tfap2a does not increase levels of melanin in mitfa hypomorphic or loss-of-function mutants. Collectively, these results show that TFAP2 paralogs, operating alongside lineage-specific transcription factors such as MITF, directly regulate effectors of terminal differentiation in melanocytes. In addition, they suggest that TFAP2A activity, like MITF activity, has the potential to modulate the phenotype of melanoma cells.
2017-02-23 | GSE67555 | GEO
Project description:bulk RNA-seq of wild-type, Gli2f/f;Gli3f/f;Wnt1-Cre, and Hand2f/f;Wnt1-Cre mouse e10.5 dissection mandibular prominences
2020-10-01 | GSE141431 | GEO
Project description:Damage to the gene regulatory network governing terminal differentiation of melanocytes leads to pigmentation phenotypes and increases the risk for melanoma. Microphthalmia-associated transcription factor (MITF) directly activates expression of melanocyte differentiation effectors, and levels of MITF have been proposed to govern the melanoma phenotype. Mutations in the gene encoding Transcription Factor Activator Protein 2 alpha (TFAP2A) cause reduced pigmentation in model organisms and premature hair graying in humans, and TFAP2A expression tends to be lower in advanced melanoma tumors than in benign nevi. However, the transcriptional targets of TFAP2A in melanocytes, and the epistatic relationship of TFAP2A and MITF, have been unclear. Using microarray-based analysis of zebrafish tfap2a mutant embryos, we generated a profile of genes whose expression is Tfap2a-dependent. We conducted anti-TFAP2A chromatin immunoprecipitation followed by next-generation sequencing (ChIP-seq) in immortalized mouse melanocytes and human primary melanocytes, and discovered that TFAP2A peaks are present near the promoters of Tfap2a-dependent genes expressed in melanocytes, and also at the majority of enhancers active in melanocytes. Comparison of TFAP2A ChIP-seq data to published MITF ChIP-seq data showed that the set of genes with promoters bound by both MITF and TFAP2A is enriched for the gene ontology term “pigment cell differentiation.” Deletion analysis of one such co-bound promoter, for Transient Receptor Potential Melastatin-like 1(TRPM1), confirmed that its expression depends on the presence of MITF binding sites as previously shown, but also depends on the presence of TFAP2A binding sites. Finally, we find that mitfa and tfap2a interact genetically in zebrafish. Collectively, these results show that TFAP2A, operating in parallel with MITF, directly regulates effectors of terminal differentiation in melanocytes and melanoma.
2017-02-17 | GSE72953 | GEO