Similar Datasets
Project description:The objective of this experiment was to determine the DNA binding site for TFAP2A in non-neural ectoderm.
2023-02-24 | GSE165712 | GEO
Project description:RNA-seq in wildtype and TFAP2A knockout non-neural ectoderm
| PRJNA695521 | ENA
Project description:DNA binding site for TFAP2A in non-neural ectoderm
| PRJNA695520 | ENA
Project description:The process of neural tube closure is a highly complex morphogenetic event that results in the generation of the primordial central nervous system. During formation of the neural tube, the non-neural ectoderm separates from the neighboring neural ectoderm and forms a single layer epithelial sheet that overlies the closed neural tube. Previous work has shown that the non-neural ectoderm is necessary for proper cranial neural tube closure, however little is known about this cell population at the molecular level or how the non-neural ectoderm contributes to neural tube closure. In this study, we used a mouse genetic system to fluorescently label the non-neural ectoderm cells and FACS sorted these cells away from the other cell populations in the neural tube. We performed high throughput RNA-sequencing to identify the transcriptome of the non-neural ectoderm and compared the gene expression profile of non-neural ectoderm cells to the remaining population of cells within the neural tube in order to identify which genes are enriched within the non-neural ectoderm. This analysis provides a clue as to which underlying molecular processes may be important for non-neural ectoderm function during neural tube closure.
2016-04-27 | GSE72059 | GEO
Project description:During vertebrate neurulation, the embryonic ectoderm is patterned into lineage progenitors for neural plate, neural crest, placodes and epidermis. Here, we use Xenopus laevis embryos to analyze the spatial and temporal transcriptome of distinct ectodermal domains in the course of neurulation, during the establishment of cell lineages. In order to define the transcriptome of small groups of cells from a single germ layer, and to retain spatial information, dorsal and ventral ectoderm was subdivided along the anterior-posterior and medial-lateral axes by microdissections. Principal Component Analysis on the transcriptomes of these ectoderm fragments primarily identifies embryonic axes and temporal dynamics. This provides a genetic code to define positional information of any ectoderm sample along the anterior-posterior and dorsal-ventral axes, directly from its transcriptome. In parallel, we use Non-Negative Matrix Factorization to predict enhanced gene expression maps onto early and mid-neurula embryos, and specific signatures for each ectoderm area. The clustering of spatial and temporal datasets allowed detection of multiple biologically relevant groups (e.g. Wnt signaling, neural crest development, sensory placode specification, ciliogenesis, germ layer specification). We provide an interactive network interface, EctoMap, for exploring synexpression relationships among genes expressed in the neurula, and suggest several strategies to use this comprehensive dataset to address questions in developmental biology as well as stem cell or cancer research.
2017-10-25 | GSE103240 | GEO
Project description:Neural tube closure in vertebrates is achieved through a highly dynamic and coordinated series of morphogenic events involving neural plate, surface ectoderm, and neural plate border. Failure of this process in the caudal region causes spina bifida. Grainyhead-like 3 (GRHL3) is an indispensable transcription factor for neural tube closure as constitutive inactivation of which leads to fully penetrant spina bifida. Here, through single-cell transcriptomics we show that at E8.5, the time-point preceding mouse neural tube closure, the co-expression of Grhl3, Tfap2a, and Tfap2c defines a previously unrecognised progenitor population of surface ectoderm. Specific deletion of Grhl3 expression using Tfap2a-Cre recapitulate the spina bifida observed in Grhl3-null animals. Moreover, conditional inactivation of Tfap2c expression in Grhl3-expressing neural plate border cells also causes mild spina bifida. These findings clearly indicate that Grhl3-expressing neural plate border cells cohort is required for the early-stage neurulation.
2024-10-09 | GSE246181 | GEO
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:The purpose of this study was to identify Tfap2a binding genome-wide in zebrafish embryos at 24hpf. Tfap2 transcription factors are essential regulators of neural crest development, melanocyte differentiation, and melanoma progression. We aimed to identify Tfap2a-occupied genes to determine direct Tfap2a-regulated transcriptional networks.
2023-12-18 | GSE250450 | GEO
Project description:A knockdown study suggested that transcription factor AP-2 alpha (Tfap2a) is required for neural crest induction in frog embryos. However, because Tfap2a is expressed in neural crest and in presumptive epidermis, a source of signals that induce neural crest, it was unclear whether this requirement is cell autonomous. Moreover, neural crest induction occurs normally in zebrafish tfap2a and mouse Tcfap2a mutant embryos, so it was unclear if a requirement for Tfap2a in this process has been evolutionarily conserved. Here we show that zebrafish tfap2c, encoding AP-2 gamma (Tfap2c), is expressed in non-neural ectoderm including transiently in neural crest. Inhibition of tfap2c with antisense oligonucleotides does not visibly perturb development. However, simultaneous inhibition of tfap2a and tfap2c utterly prevents neural crest induction, supporting a conserved role for Tfap2-type activity in neural crest induction. Transplant studies suggest that this role is cell-autonomous. In addition, in tfap2a/tfap2c doubly deficient embryos cranial placode derivatives are reduced, although gene expression characteristic of pre-placodal domain is normal. Unexpectedly, Rohon-Beard sensory neurons, which previous studies indicated are derived from the same precursor population as neural crest, are reduced by less than half in such embryos, implying a non-neural crest origin for a subset of them.
| S-EPMC1904501 | biostudies-literature
Project description:The aim of this study is to compare the transcriptome profiles between wild type (WT, B6N in this case), with mutant mice (Tfap2a+/- or Tfap2b+/- respectively)
2020-08-04 | GSE155629 | GEO