E-GEOD-63810
Ontology highlight
ABSTRACT:
OTHER RELATED OMICS DATASETS IN: PRJNA269130
PROVIDER: E-GEOD-63810 | ExpressionAtlas | 2019-05-14
REPOSITORIES: ExpressionAtlas
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| E-GEOD-63810-analysis-methods.tsv | Tabular | |||
| E-GEOD-63810-analytics.tsv | Tabular | |||
| E-GEOD-63810-analytics.tsv.undecorated | Tabular | |||
| E-GEOD-63810-analytics.tsv.undecorated.unrounded | Tabular | |||
| E-GEOD-63810-analytics.tsv.unrounded | Tabular |
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Project description:We report the single base pair analysis of the ocular transcriptome from wild type and BC027072 knockout animals. Comparison was analyzed to understand gene expression changes in a mouse model for early onset retinal degeneration which phenocopies a human form of autosomal recessive retinitis pigmentosa Eye mRNA profiles were generated from 3 week-old C57BL/6J and BC027072 -/- in triplicate and sequenced using the Illumina HiSeq 2500
2015-02-03 | E-GEOD-63810 | biostudies-arrayexpress
Project description:We report the single base pair analysis of the ocular transcriptome from wild type and BC027072 knockout animals. Comparison was analyzed to understand gene expression changes in a mouse model for early onset retinal degeneration which phenocopies a human form of autosomal recessive retinitis pigmentosa
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Project description:We performed unbiased transcriptional profiling in an adult-onset Pkd2 mouse model at an early stage before cysts formed using as controls wild type and PC2+cilia double knockout mice which are protected from ADPKD. By a tripartite comparison, we identified differetially expressed genes which have significant different expression in Pkd2-only knockout with same direction of change from both wild type and Pkd2+Cilia double knockout.
2020-12-31 | GSE149739 | GEO
Project description:The initial aim of this work was to understand the pathophysiology of Enhanced S-cone Syndrome (ESCS) that leads to retinal degeneration. Although ESCS was identified in humans decades ago and since then the causative genes have been elucidated, our understanding of the accompanying retinal degeneration is still poorly understood. Knockout of the Nrl transcription factor in mice produces a retina overpopulated with S-cone like photoreceptors along with absence of rod photoreceptors and recapitulates many of the phenotypic features seen in human ESCS patients. We wanted to study this murine model through a combinatorial genetic and structural approach to improve understanding of the disease process that leads to photoreceptor degeneration and blindness, potentially guiding future therapies. By using RNA-Sequencing (RNA-Seq) to examine mature wild type and Nrl-/- ocular tissues, we were able to determine global changes in their transcriptomes. The massively parallel RNA-sequencing experiment revealed new insight into the transcriptional mis-regulation in the ESCS murine model and revealed a change in gene expression in putative proteins involved in photoreceptor phagocytosis. Key photoreceptor ligands necessary for phagocyotsis, Tub and Tulp1, were down-regulated in the Nrl-/- retina. Down regulation of key retinoid metabolic genes, coupled with down-regulation of Tub and Tulp1, suggested a potential mechanism involving defective phagocytosis underlies the photoreceptor degeneration seen in ESCS. We report RNA-Seq experiments of whole eye and retinal tissues from wild type and Nrl transcription factor knockout mice on the C57BL/6 background. Examine two different ocular tissues in two mouse models of varying photoreceptor populations
2011-06-07 | E-GEOD-29752 | biostudies-arrayexpress
Project description:The early retinal progenitor-expressed gene Sox11 regulates the timing of the differentiation of retinal cells. Sry-related HMG box (Sox) proteins play diverse and critical roles in a variety of morphogenetic processes during embryonic development. Sox11 and Sox4 are members of the SoxC subtype, and we found that Sox11 was strongly expressed in early retinal progenitor cells, and that when expression of Sox11 subsided around birth, Sox4 expression began. To analyze the role of Sox11 and Sox4 in retinal development, we perturbed their expression pattern by expressing them ectopically in retinal explant culture. Overexpression of Sox11 or Sox4 in retinal progenitors resulted in similar phenotypes, that is, increased cone cells and decreased Muller glia. Sox11-knockout retinas showed delayed onset and progress of differentiation of early-born retinal cells during the embryonic period. After birth, retinal differentiation took place relatively normally, probably because of the redundant activity of Sox4, which starts to differentiate around birth. Neither overexpression nor loss-of-function analysis gave any evidence that Sox11 and Sox4 directly regulate transcription of genes critical to early-born retinal cells. However, histone H3 acetylation status of the early neurogenic genes was lowered in knockout retinas, suggesting that Sox11 regulates the timing of differentiation in early-born retinas by creating an epigenetic state that helps to establish the competency to differentiate. We also found that the unique expression patterns of Sox11 and Sox4 may be achieved by the Notch signaling pathway and by epigenetic regulation. Taking our findings together, we propose that the precise regulation of Sox11 and Sox4 expression during retinogenesis by multiple mechanisms leads to the fine adjustment of retinal differentiation. To delineate the molecular mechanisms underlying the retinal action of Sox11, we performed microarray analysis of E18 retinas from wild-type and Sox11 knockout mice. Total RNA was obtained from each one retina of Sox11 knockout and wild-type littermate embryos at E18.
2012-12-28 | E-GEOD-43089 | biostudies-arrayexpress
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2016-03-23 | E-GEOD-77403 | biostudies-arrayexpress
Project description:Eye photoreceptor membrane discs in outer rod segments are highly enriched in the visual pigment rhodopsin and the omega-3 fatty acid docosahexaenote (DHA). The eye acquires DHA from blood, but transporters for DHA uptake across the blood-retinal barrier (BRB) or retinal pigment epithelium have not been identified. Mfsd2a is a newly described sodium-dependent lysophosphatidylcholine symporter expressed at the BRB. Microarrays were used to determine difference in gene expression between wild-type and Mfsd2a KO eye cups.
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Project description:Purpose: The purpose of this study was to use RNA-seq to investigate the molecular mechanisms of damage in the early stages of the response to axonal injury, before the onset of RGC death. Methods: 12-week-old wild-type (WT) mice were used in this study. The experiment group underwent an optic nerve crush (ONC) procedure to induce axonal injury in the right eye, and the control group underwent a sham procedure. Retinal mRNA profiles were generated by deep sequencing, in triplicate, using IlluminaHiseq2000. The sequence reads were analyzed by CLC genomics workbench and R software. qRT–PCR validation was performed using TaqMan assays. Results: Using an optimized data analysis workflow, we mapped about 66 million sequence reads per sample to the mouse genome (build mm9). Differential gene expression analysis showed that endoplasmic reticulum stress-related genes and antioxidative response-related genes have been shown to be significantly upregulated 2 days after ONC. Conclusions: Our study represents the first detailed analysis of retinal transcriptomes in the early stages after axonal injury. Our results indicated that ER stress plays a key role under these conditions. Furthermore, the antioxidative defense and immune responses occurred concurrently in the early stages after axonal injury. We believe that our study will lead to a better understanding of and insight into the molecular mechanisms underlying RGC death after axonal injury. Retinal mRNA profiles of 12 week-old wild type (WT) after ONC or sham were generated by deep sequencing, in triplicate, using Illumina Hiseq2000.
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