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

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

PROVIDER: PRJNA564851 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR10097036_1.fastq.gz	Fastqsanger.gz
	SRR10097036_2.fastq.gz	Fastqsanger.gz
	SRR10097037_1.fastq.gz	Fastqsanger.gz
	SRR10097037_2.fastq.gz	Fastqsanger.gz
	SRR10097038_1.fastq.gz	Fastqsanger.gz

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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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miR-302 is a temporal regulator of neural crest development [Mouse miRNA-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 miRNA differences during neural crest development

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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

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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 [Chicken miRNA-seq]

Project description:expression of miR-302 was analyzed in chicken embryos using small RNA-seq to verify an increase or decrease in exppression when miR-302 was overexpressed or knocked down

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miR-302 is a temporal regulator of neural crest development

Project description:This SuperSeries is composed of the SubSeries listed below.

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

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 | GSE216136 | GEO

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

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miR-302-367 regulates cardiomycyte proliferation and differentiation during development

Project description:To define the role of miR-302-367 cluster in cardiac development, we overexpressed miR-302-367 cluster in mouse heart by using R26R-miR-302-367; Nkx2.5-Cre mice. This data set contains the microarrays examining gene expression in the hearts of R26R-miR-302-367; Nkx2.5-Cre mice at postnatal day 14.

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