The role of Atf4 in the embryonic lens at E16.5
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA852087 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR19793406_1.fastq.gz | Fastqsanger.gz | |||
| SRR19793406_2.fastq.gz | Fastqsanger.gz | |||
| SRR19793407_1.fastq.gz | Fastqsanger.gz | |||
| SRR19793407_2.fastq.gz | Fastqsanger.gz | |||
| SRR19793408_1.fastq.gz | Fastqsanger.gz |
Items per page: 5 1 - 5 of 18 |
Similar Datasets
Project description:Transcriptome analysis reporting genes that are differentially expressed as a result of knockout of the gene ATF4.
2023-12-08 | GSE206760 | GEO
Project description:We applied previously established in silico whole-embryo body (WB)-subtraction-based approach to identify “lens-enriched” genes. These new RNA-seq datasets on embryonic stages E10.5, E12.5, E14.5 and E16.5 confirmed high expression of established cataract-linked genes and identified several new potential regulators in the lens. Finally, we present lens stage-specific UCSC Genome Brower annotation-tracks; these are publicly accessible through iSyTE (https://research.bioinformatics.udel.edu/iSyTE/) and enable a user-friendly visualization of lens gene expression/enrichment to help prioritize genes from high-throughput data from cataract cases.
2019-01-08 | GSE119596 | GEO
Project description:Conditional disruption of Klf4 in the ectoderm-derived tissues of the eye results in defective cornea, conjunctiva and the lens. Expression of Klf4 is first detected in the embryonic day-12 (E12) mouse lens, peaks at E16, and declines thereafter. Lenses from Mice which were conditional null for Klf4 (Klf4CN) were characterized by morphology and transcriptome. Wild type and Klf4-conditional null mouse lens gene expression at embryonic day 16.5 (E16.5) and postnatal day 56 (PN56) was surveyed using Affymetrix mouse whole genome 430 2 arrays.
2013-07-01 | E-GEOD-47694 | biostudies-arrayexpress
Project description:Oxidative stress is pathogenic in neurological diseases including stroke. The identity of oxidative stress-inducible transcription factors and their role(s) in propagating the death cascade are poorly understood. Microarray analysis of neurons undergoing oxidative stress showed significant induction of prodeath genes. These genes have been shown to be regulated by the bZip transcription factor, ATF4. ATF4 protein localized to the promoter of a putative death gene in neurons in vitro and in vivo. Germline deletion of ATF4 in neurons resulted in a reduction in oxidative stress-induced gene expression and resistance to oxidative death. ATF4 knockout mice experienced significantly smaller infarcts and improved behavioral recovery as compared to wild-type mice subjected to the same reductions in blood flow in a rodent model of stroke. ATF4 modulates an early, upstream event in the death pathway, as resistance to oxidative death by ATF4 deletion was associated with decreased consumption of the antioxidant glutathione. Restoration of ATF4 protein in knockout neurons was sufficient to restore sensitivity to oxidative death and to reaccelerate loss of glutathione. Together, these findings establish ATF4 as a redox-regulated, pro-death transcriptional activator in the nervous system that propagates death responses to oxidative stress in vitro and to stroke in vivo. Keywords: ATF4, oxidative stress, gene expression, neuroprotection, stroke WT and ATF4 KO embryonic neurons were studied. Untreated neurons (no=8 per genotype) and neurons challenged with oxidative stress with the glutamate homolog homocysteate (HCA, no=4 per genotype) were studied, for a total of 24 samples.
2010-06-25 | E-GEOD-10470 | biostudies-arrayexpress
Project description:RNA sequencing of mice E16.5 whole embryonic testes
| PRJEB8332 | ENA
Project description:Gata3 is a DNA-binding transcription factor involved in cellular differentiation in a variety of tissues. To investigate the role of Gata3 in lens development we conducted lens-specific conditional loss-of-function model of Gata3 and confirmed abnormal regulation of cell cycle exit-coupled lens differentiation and retention of nuclei in the mutated lens fibers. We analyzed transcriptomes between control and mutated lenses by RNA-seq and revealed dysregulation of genes encoding critical components of the lens differentiation cascade, including a subset of crystallin genes, down-regulation of Dnase2b and reduced expression of Cdkn1b/p27 and Cdkn1c/p57.
2020-01-08 | GSE131291 | GEO
Project description:This trancriptome analysis reports genes that are differentially expressed upon deletion of the fibronectin gene from the lens during late embryonic development.
2020-07-08 | GSE119878 | GEO
Project description:Purpose: While the bioinformatics gene-discovery tool iSyTE (integrated Systems Tool for Eye gene discovery) has proved effective in identifying new cataract-linked genes, it primarily depended on lens-enriched expression of just three wild-type mouse embryonic stages. To increase iSyTE’s efficacy, a broad range of embryonic (E) and postnatal (P) lens microarray datasets from wild-type and specific gene-perturbation mutant mice were analyzed and a new web-interface was developed for their effective access and downstream-analysis. Methods: Five new mouse lens microarrays were generated and analyzed with all publicly available Affymetrix and Illumina lens datasets representing the stages E9.5, E10.25, E10.5, E11.5, E12.5, E15.5, E16.5, E17.5, E19.5, P0, P2, P4, P8, P12, P20, P28, P30, P42, P52, P56, P60 and mouse mutants for the genes: Brg1, CBP:p300, E2f1:E2f2:E2f3, Foxe3, Hsf4, Klf4, Mafg:Mafk, Notch2, Pax6, Sparc, Tdrd7. Results: The integrated lens microarray analysis accurately reflects established gene expression patterns and defines a new lens-signature gene-set for embryonic and postnatal stages that includes several novel candidates namely, Grifin, Ogn, Fabp5, Mboat1, Tmem40, Dhx32, Aldoc, Pgam2, Hmgn3, Mocs2, Gprc5b, Gstm1, Npl, and Zbtb8b. Combined analyses of 32 developmental/genetic data-conditions identifies several new transcription and signaling factors that potentially function in lens development and/or homeostasis. Conclusions: The updated iSyTE web-interface: (1) comprehensively informs on normal lens developmental and cataract-associated transcriptome dynamics and identifies new high-priority candidates for these processes, and (2) offers user-friendly visualization.
2017-09-21 | GSE100136 | GEO
Project description:Genome-wide approach to identify the cell-autonomous role of Brg1 in lens fiber cell terminal differentiation. To examine roles of Brg1 in mouse lens development, a dnBrg1 transgenic construct was expressed using the lens-specific alphaA-crystallin promoter in postmitotic lens fiber cells. Morphological studies revealed abnormal lens fiber cell differentiation in transgenic lenses resulting in cataract. Electron microscopic studies showed abnormal lens suture formation and incomplete karyolysis (denucleation) of lens fiber cells. To identify genes regulated by Brg1, RNA expression profiling was performed in E15.5 embryonic wild type and dnBrg1 transgenic lenses. In addition, comparisons between differentially expressed genes in dnBrg1 transgenic, Pax6 heterozygous, and Hsf4 homozygous lenses identified multiple genes co-regulated by Brg1, Hsf4 and Pax6. Among them DNase IIbeta, a key enzyme required for lens fiber cell denucleation, was found downregulated in each of the Pax6, Brg1 and Hsf4 model systems. Lens-specific deletion of Brg1 using conditional gene targeting demonstrated that Brg1 was required for lens fiber cell differentiation and indirectly for retinal development but was not essential for lens lineage formation. Wild type and dnBrg1 transgenic lenses, 4 biological replicates each
2011-01-01 | E-GEOD-22322 | biostudies-arrayexpress
Project description:During oncogenic transformation, cells acquire genetic mutations that override the normal mechanisms regulating cellular proliferation. Excessive expression of activating transcription factor 4 (ATF4) is often observed in mammalian malignant tumors. However, little is known about the role of ATF4 in the malignant transformation of normal cells. Here, we show that ATF4 promotes oncogene-induced malignant transformation of murine fibroblasts by suppressing the expression of cellular senescence-associated genes. Ectopic expression of oncogenes, H-rasV12 and simian virus 40 large T-antigen, elicited malignant transformation of embryonic fibroblasts from wild-type mice, but not from Atf4-null (Atf4-/-) mice. The oncogenic stresses induced the expression of both Atf4 and cyclin-dependent kinase inhibitor 2a (Cdkn2a), in wild-type cells. Elevated levels of ATF4 successively suppressed the expression of cdkn2a encoding the cellular senescence-associated proteins, p16INK4a and p19ARF, thereby promoting oncogenic transformation. Conversely, the loss of ATF4 caused cellular senescence resulting from the consistent expression of p16INK4a and p19ARF. These findings reveal a novel function of ATF4: that of promoting oncogenic transformation by suppressing cellular senescence. Total 2 samples were derived from [1] H-Ras and SV40T expressing vector-transfected wild-type mouse embryonic fibroblasts (MEFs) and [2] H-Ras and SV40T expressing vector-transfected Atf4-/- MEFs
2011-08-16 | E-GEOD-31405 | biostudies-arrayexpress