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E-MTAB-6133

ABSTRACT: RNAseq analysis of Chrnb4-cre driven Dicer conditional knockout (Dicer CKO) whole retinas

PROVIDER: E-MTAB-6133 | ExpressionAtlas | 2019-01-21

REPOSITORIES: ExpressionAtlas

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			Action	DRS
	E-MTAB-6133-analysis-methods.tsv	Tabular
	E-MTAB-6133-analytics.tsv	Tabular
	E-MTAB-6133-atlasExperimentSummary.Rdata	Rdata
	E-MTAB-6133-configuration.xml	Xml
	E-MTAB-6133-g2_g1-mvaPlot.png	Other

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RNAseq analysis of Chrnb4-cre driven Dicer conditional knockout (Dicer CKO) whole retinas

Project description:RNAseq analysis of Chrnb4-cre driven Dicer conditional knockout (Dicer CKO) whole retinas

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miRNAseq analysis of Chrnb4-cre driven Dicer conditional knockout (Dicer CKO) whole retinas

Project description:miRNAseq analysis of Chrnb4-cre driven Dicer conditional knockout (Dicer CKO) whole retinas

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RNAseq analysis of Chrnb4-cre driven Dicer conditional knockout (Dicer CKO) whole retinas

Project description:We have shown that Chrnb4-cre; Dicerflox/flox retinas (Dicer CKO) display a cone dystrophy by postnatal day P21, independent of rod degeneration. To elucidate which gene pathways were affected by Dicer loss, RNA sequencing was performed in whole neural retinas of P21 control and Dicer CKO mice. This experiment aims to identify which genes were differentially expressed between Dicer conditional knockout and control mice.

2019-01-14 | E-MTAB-6133 | biostudies-arrayexpress

miRNAseq analysis of Chrnb4-cre driven Dicer conditional knockout (Dicer CKO) whole retinas

Project description:We have shown that Chrnb4-cre; Dicerflox/flox retinas (Dicer CKO) display a cone dystrophy by postnatal day P21, independent of rod degeneration. To elucidate which miRNAs were involved in such phenotype, miRNA sequencing was performed in whole retinas of P21 and 3.5 month old control and Dicer CKO mice. This experiment aims to identify which miRNAs were differentially expressed in Dicer conditional knockout mice when compared to control mice.

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Analysis of gene expression in wildtype and Notch1 mutant retinal cells by single cell profiling

Project description:Loss of Notch1 in retinal progenitor cells (RPCs) during postnatal retinal development results in the overproduction of rod photoreceptors at the expense of interneurons and glia. To examine the molecular underpinnings of this observation, microarray analysis of singla retinal cells from wildtype (WT) or Notch1 conditional knockout (N1-CKO) retinas was performed. The majority of N1-CKO cells lost expression of known Notch target genes. These cells also had low levels of RPC and cell cycle genes, and robustly upregulated rod precursor genes. In addition, single WT cells, in which cell cycle marker genes were downregulated, expressed markers of both rod photoreceptors and interneurons. These results demonstrate that individual, newly postmitotic retinal cells can begin to differentiate into more than one cell type, and that this transitional state may be dependent on Notch1 signaling. We used microarrays to examine gene expression changes that occur in single cells after the removal of Notch1 during retinal development. Retinas of Notch1fl/fl P0 pups were electroporated in vivo with plamids encoding Cre driven by a broadly active promoter, CAG, along with a Cre-responsive GFP reporter, also driven by CAG promoter (CALNL-GFP). For controls, the retinas of sibling Notch1fl/fl pups were electroporated with CAG:GFP. The animals were sacrificed at P3 to allow time for Notch1 to be genetically removed and downstream gene expression changes to occur. Retinas electroporated with either CAG;Cre and CALNL-GFP or CAG:GFP alone were dissected and dissociated to individual cells, which were harvested under a dissecting microscope on the basis of their GFP signal.

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small RNAseq analysis of the global retinal transcriptome of rod photoreceptor-specific Dicer1 conditional knockout mice and control littermates

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