Single-cell, clonal and spatial atlases of neural plate border and neurogenic placodes illuminate their specification and evolution.
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ABSTRACT:
ORGANISM(S): Mus musculus
PROVIDER: GSE318565 | GEO | 2026/04/07
REPOSITORIES: GEO
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Project description:Single-cell, clonal and spatial atlases of neural plate border and neurogenic placodes illuminate their specification and evolution.
| PRJNA1419233 | ENA
Project description:Purpose: The goal of this study is to identify similarities and differences in the induction of the central nervous system and the sensory placodes in chick. Method: mRNA profiles for central and anterior pre-steak epiblast, neural plate, anterior and posterior pre-placodal region, non-neural epiblast, gastrula stage area opaca exposed to Hensen's node for 5 hours and control area of opaca from the same stage. Deep sequencing was carried with Illumina HiSeq 2000. After filtering low quality reads, alignment was carried using TopHat2, differential expression analysis was done using R-package (easyRNA-seq and DSEq). Results: Despite the differences in inducing tissues (i.e. node and lateral head mesoderm) and in the final outcome (neural plate and pre-placodal region), the initial set of genes induced by both tissues is largely identical. We define this transcriptional signature as 'pre-neural state', and demonstrate its functional significance for both inductive processes. An unbiased approach using GENEI3 and community clustering reveals the gene regulatory modules characterising the transcirptional states of pre-neural, neural and placodal cells. Conclusion: Induction of the neural plate and the pre-placodal region initially share common features, and diverge later. The pre-neural state is similar to the neural plate border and pre-streak epiblast state.
2018-02-14 | GSE106346 | GEO
Project description:The otic placode, from which the inner ear develops, initially forms as a thickened ectodermal patch adjacent to the dorsolateral hindbrain. Induction of otic placodal cells from human pluripotent stem cells (hPSCs) provides a robust approach to investigation of otic development. However, attempts to recapitulate otic lineage specification from hPSCs by stepwise differentiation methods have had limited success. One possible reason is that the role of signaling pathways in otic cell differentiation is not fully understood. Here, we developed a novel differentiation system involving use of suspension culture (3D floating culture) in combination with signaling factors for generating otic placodal cells via stepwise differentiation of hPSCs. We demonstrate that hPSC-derived pre-placodal cells acquired the potential to differentiate into posterior placodal cells after fibroblast growth factor 2 (FGF2) and retinoic acid (RA) treatment. Subsequent activation of WNT signaling following posterior placode specification induced differentiation of SIX1+/PAX8+/SOX2+ otic placodal cells. qPCR analysis showed that WNT activation increased expression of otocyst markers, including PAX8, PAX2, DLX5 and FBXO2. Moreover, induced otic cells exhibited similar gene expression patterns to the ventral and medial portions of the otocyst that give rise to the sensory epithelium of the inner ear. Collectively, our results indicate a critical role for FGF2, RA, and WNT signaling for the in vitro differentiation of the otic cell lineage from hPSCs. Our new culture system paves the way for improved modeling of early human inner ear development and will be of value to studies on the further differentiation of sensory epithelial cells.
2022-02-01 | GSE175998 | GEO
Project description:Poly(ADP-ribose) polymerase 3 (PARP3) is a member of the PARP family of enzymes. It is structurally related to the well characterized type member PARP1 that orchestrates DNA strand break repair and cell death by the synthesis of poly(ADP-ribose). In contrast, the functions of PARP3 are undefined. We have used several in vitro and in vivo approaches to examine the possible functions of PARP3 as a transcriptional regulator, a function suggested from its previously reported association with several Polycomb group (PcG) proteins. A ChIP-chip analysis of PARP3 gene occupancy in the human neuroblastoma cell line SK-N-SH reveals that PARP3 is preferentially associated with developmental genes and is significantly enriched around the transcriptional start site of several genes encoding neuronal and sensory placodes specifiers, such as SOX9, DLX3 and DLX4. Using zebrafish as a vertebrate animal model, we demonstrate that Parp3 plays a key role in ectodermal and neural crest specification. Morpholino oligonucleotide-directed inhibition of parp3 expression in zebrafish impairs the expression of the neural crest cell specifier sox9a and of dlx3b/dlx4b, the formation of cranial sensory placodes, inner ears and pectoral fins. It delays pigmentation and severely impedes the development of the median fin fold and tail bud. Our findings demonstrate that Parp3 is crucial in the early stages of zebrafish development, possibly by exerting its transcriptional regulatory functions as early as during the specification of the neural plate border.
2011-08-18 | GSE23709 | GEO
Project description:Poly(ADP-ribose) polymerase 3 (PARP3) is a member of the PARP family of enzymes. It is structurally related to the well characterized type member PARP1 that orchestrates DNA strand break repair and cell death by the synthesis of poly(ADP-ribose). In contrast, the functions of PARP3 are undefined. We have used several in vitro and in vivo approaches to examine the possible functions of PARP3 as a transcriptional regulator, a function suggested from its previously reported association with several Polycomb group (PcG) proteins. A ChIP-chip analysis of PARP3 gene occupancy in the human neuroblastoma cell line SK-N-SH reveals that PARP3 is preferentially associated with developmental genes and is significantly enriched around the transcriptional start site of several genes encoding neuronal and sensory placodes specifiers, such as SOX9, DLX3 and DLX4. Using zebrafish as a vertebrate animal model, we demonstrate that Parp3 plays a key role in ectodermal and neural crest specification. Morpholino oligonucleotide-directed inhibition of parp3 expression in zebrafish impairs the expression of the neural crest cell specifier sox9a and of dlx3b/dlx4b, the formation of cranial sensory placodes, inner ears and pectoral fins. It delays pigmentation and severely impedes the development of the median fin fold and tail bud. Our findings demonstrate that Parp3 is crucial in the early stages of zebrafish development, possibly by exerting its transcriptional regulatory functions as early as during the specification of the neural plate border. ChIP were conducted as described (Rodrigue et al. 2006). PARP3 was immunoprecipitated from 3 x 10^7 SK-N-SH cells with a commercial anti-PARP3 (Enzo Life Sciences ALX-210-541). In control ChIP, PARP3 antibodies were replaced by rabbit IgG. Two independent PARP3 and control ChIP-chip experiments were achieved. The DNA was amplified using LM-PCR and labelled with Cy5 (PARP3) and Cy3 (IgG) before hybridization on Agilent Human promoter arrays (two 244k chip per ChIP for a total of 4 chips). Detailed protocols can be found at http://www.ircm.qc.ca/microsites/francoisrobert/en. Regions significantly enriched for PARP3 relative to IgG were identified as described (Lee et al. 2006).
2011-08-17 | E-GEOD-23709 | biostudies-arrayexpress
Project description:Purpose: Understand how the misexpression of key sensory cell determinant POU IV affects cell type specification of various sensory neurons in the peripheral nervous system in Ciona. Methods: CesA>POU IV (2.5ng/l) + CesA>GFP (5.0ng/l) injected eggs and control eggs were fertilized side by side, and allowed to develop to the late tailbud stage (13.5h after fertilization at 18°C). For each sample, 120 morphologically normal embryos were used for single cell RNA-seq assays. Dissociation of the embryos and single cell RNA-seq assays by 10x Genomics chromium system were done as described in 9. Horie R. et al., Shared evolutionary origin of vertebrate neural crest and cranial placodes. Nature 560, 228-232 (2018). Results: Misexpression of POU IV leads to the formation of Synthetic Cell Types that exhibit properties of other sensory neurons, especially those of bipolar tail neurons (BTNs) and a synthetic gene battery that is not found in any wildtype sensory neuron.
2021-12-29 | GSE192645 | GEO
Project description:Development of the vertebrate head is a complex and dynamic process, which requires integration of all three germ layers and their derivatives. Of special importance are ectoderm-derived cells that form the cranial placodes, which then differentiate into the cranial ganglia and sensory organs. Critical to a fully functioning head, defects in cranial placode and sensory organ development can result in congenital craniofacial anomalies. In a forward genetic screen aimed at identifying novel regulators of craniofacial development, we discovered an embryonically lethal mouse mutant, snouty, which exhibits malformation of the facial prominences, cranial nerves and vasculature. The snouty mutation was mapped to a single nucleotide change in a ubiquitously expressed gene, Med23, which encodes a subunit of the global transcription co-factor complex, Mediator. This experiment examines transcriptional differences between Med23 mutant mice and their wt littermates at embryonic day 9.5.
2020-01-28 | GSE144327 | GEO
Project description:The embryonic ectoderm gives rise to four fates: neural, neural crest, placodal and epidermal. The derivatives of these fates give rise to the entire vertebrate nervous system and skin. To explore how these cell fates emerge, we profiled single cell chromatin accessibility in the chick embryonic ectoderm at five developmental timepoints.
2025-12-02 | GSE271424 | GEO
Project description:Vertebrate Hox genes are key players in the establishment of structures during the development of the main body axis. Subsequently, they play important roles either in organizing secondary axial structures such as the appendages, or during homeostasis in postnatal stages and adulthood. Here we set up to analyze their elusive function in the ectodermal compartment, using the mouse limb bud as a model. We report that the HoxC gene cluster was globally co-opted to be transcribed in the distal limb ectoderm, where it is activated following the rule of temporal colinearity. These ectodermal cells subsequently produce various keratinized organs such as nails or claws. Accordingly, deletion of the HoxC cluster led to mice lacking nails (anonychia) and also hairs (alopecia), a condition stronger than the previously reported loss of function of Hoxc13, which is causative of the ectodermal dysplasia 9 (ECTD9) syndrome in human patients. We further identified, in mammals only, two ectodermal-specific enhancers located upstream the gene cluster, which act synergistically to regulate Hoxc genes in these ectodermal organs. Deletion of these enhancers alone or in combination revealed a strong quantitative component in the regulation of these genes in the ectoderm, suggesting that these two enhancers may have evolved along with mammals to provide the level of HOXC proteins necessary for the full development of hairs and nails.
2020-10-05 | GSE150701 | GEO
Project description:Vertebrate Hox genes are key players in the establishment of structures during the development of the main body axis. Subsequently, they play important roles either in organizing secondary axial structures such as the appendages, or during homeostasis in postnatal stages and adulthood. Here we set up to analyze their elusive function in the ectodermal compartment, using the mouse limb bud as a model. We report that the HoxC gene cluster was globally co-opted to be transcribed in the distal limb ectoderm, where it is activated following the rule of temporal colinearity. These ectodermal cells subsequently produce various keratinized organs such as nails or claws. Accordingly, deletion of the HoxC cluster led to mice lacking nails (anonychia) and also hairs (alopecia), a condition stronger than the previously reported loss of function of Hoxc13, which is causative of the ectodermal dysplasia 9 (ECTD9) syndrome in human patients. We further identified, in mammals only, two ectodermal-specific enhancers located upstream the gene cluster, which act synergistically to regulate Hoxc genes in these ectodermal organs. Deletion of these enhancers alone or in combination revealed a strong quantitative component in the regulation of these genes in the ectoderm, suggesting that these two enhancers may have evolved along with mammals to provide the level of HOXC proteins necessary for the full development of hairs and nails.
2020-10-05 | GSE150700 | GEO