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MiR-302 is a temporal regulator of neural crest development [Mouse miRNA-seq]

ABSTRACT: We analyzed wildtype and miR-302 knockout embryos at E7.5 and sorted neural crest using Wnt1-Cre at E8.5 and Sox9 at E9.5 to capture miRNA differences during neural crest development

ORGANISM(S): Mus musculus

PROVIDER: GSE137240 | GEO | 2020/03/09

REPOSITORIES: GEO

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miR-302 is a temporal regulator of neural crest development [Mouse RNA-seq]

Project description:We analyzed wildtype and miR-302 knockout embryos at E7.5 and sorted neural crest using Wnt1-Cre at E8.5 and Sox9 at E9.5 to capture transcriptomic differences during neural crest development

2020-03-09 | GSE137227 | GEO

Post-transcriptional regulation in cranial neural crest cells expands developmental potential [I]

Project description:Developmental potential is progressively restricted after germ layer specification during gastrulation. However, cranial neural crest cells challenge this paradigm, as they develop from anterior ectoderm yet give rise to both mesodermal derivatives of the craniofacial skeleton and ectodermal derivatives of the peripheral nervous system. How cranial neural crest cells differentiate into multiple lineages is poorly understood. Here, we demonstrate that cranial neural crest cells possess a transient state of increased chromatin accessibility; and that the earliest premigratory neural crest are biased towards either a neuronal or ectomesenchymal fate, with each lineage expressing distinct factors from the pluripotent state. We profile the spatiotemporal emergence of each neural crest population and demonstrate that the ectomesenchymal lineage forms prior to the neuronal progenitors. Expression of the pluripotency microRNA family miR-302 is maintained in cranial neural crest cells and genetic deletion leads to precocious specification of the ectomesenchymal lineage. We find that miR-302 directly targets Sox9 to slow the timing of ectomesenchyme induction and regulates multiple genes involved in chromatin condensation to maintain accessibility for neuronal differentiation. Loss of mir-302 results in reduced chromatin accessibility in the neuronal progenitor lineage of neural crest and a reduction in peripheral neuron differentiation. Our findings reveal a post-transcriptional mechanism governed by miRNAs from pluripotency as an important mechanism to expand developmental potential of cranial neural crest.

2022-10-25 | GSE215977 | GEO

Post-transcriptional regulation in cranial neural crest cells expands developmental potential [II]

2022-10-25 | GSE216136 | GEO

Expression analysis of miR-302 knockout and wild-type embryos during neurulation

Project description:Wild-type or miR-302 knockout tissue was isolated from embryos during neurulation in replicate Performed in biological triplicate except for E7.5 WT which was in duplicate and E9.5 timepoints which were in quadruplicate. Biological replicate samples represent independent embryos. Total RNA collected with Trizol. All processing conducted at the UCLA Neuroscience Genomics Core. MouseRef-8 v2.0 Expression BeadChips.

2015-08-03 | E-GEOD-62396 | biostudies-arrayexpress

miR-302 is a temporal regulator of neural crest development

Project description:miR-302 is a temporal regulator of neural crest development

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Single cell gene expression of early E8.5 pioneer neural crest cells and paraxial mesoderm

Project description: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. At E8.5, as migrating neural crest cells begin to exit the neural fold/epidermal ectoderm boundary, we examined the facial mesenchyme, composed of neural crest and paraxial mesoderm cells, as well as cells from adjacent neuroepithelium We performed single cell studies to better define the gene expression states of the early E8.5 pioneer neural crest cells and paraxial mesoderm, and present microarray data detailing expression patterns within these embryonic cell populations. Mouse emrbyos were harvested at developmental stage E8.5 and single cells were captured from the neuroepithilium, neural crest, and paraxial mesoderm. RNA was extracted, labelled, and quantified using the Mouse ST-l microarray.

2014-03-18 | E-GEOD-55964 | biostudies-arrayexpress

miR-302 is a temporal regulator of neural crest development [Chicken miRNA-seq]

Project description:miR-302 is a temporal regulator of neural crest development [Chicken miRNA-seq]

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miR-302 is a temporal regulator of neural crest development [Mouse miRNA-seq]

Project description:miR-302 is a temporal regulator of neural crest development [Mouse miRNA-seq]

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miR-302 is a temporal regulator of neural crest development [Mouse RNA-seq]

Project description:miR-302 is a temporal regulator of neural crest development [Mouse RNA-seq]

| PRJNA564851 | ENA

Effect of SOX9 depletion on transcription mRNA in hESC-derived cranial neural crest cells [SLAM-seq]

Project description:To assess the effects of SOX9 depletion on transcription in hESC-derived cranial neural crest cells, we performed genome editing of the H9 hESC lines to tag SOX9 with FKBPV36, V5, and mNeonGreen. Upon differentiating edited hESC to cranial neural crest cells using an established protocol, addition of the degrader molecule dTAGV-1 results in SOX9 depletion. We then profiled transcription by metabolic labeling of RNA (SLAM-Seq) in undepleted CNCCs or CNCCs in which SOX9 was depleted for 3h or 24h

2022-07-04 | GSE205903 | GEO

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