Eye development
Ontology highlight
ABSTRACT:
PROVIDER: PRJEB29741 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Eye development in mouse and rat
| PRJNA87185 | ENA
Project description:Gene expression profiling of zebrafish early eye development on 3 to 5 days post fertilization (dpf)
2012-12-31 | GSE19320 | GEO
Project description:Gene expression profiling of zebrafish early eye development on 3 to 5 days post fertilization (dpf) Gene expression on 3 to 5 dpf eyes were compared. Each sample contains three replicates.
2012-12-31 | E-GEOD-19320 | biostudies-arrayexpress
Project description:Mutations in Peroxidasin (PXDN) cause severe inherited eye disorders in humans, such as congenital cataract, corneal opacity, and developmental glaucoma. The role of peroxidasin during eye development is poorly understood. Here we describe the first Pxdn mouse mutant which was induced by ENU (N-ethyl-N-nitrosourea) and led to a recessive phenotype. Sequence analysis of cDNA revealed a T3816A mutation resulting in a premature stop codon (Cys1272X) in the peroxidase domain. This mutation causes severe anterior segment dysgenesis and microphthalmia resembling the manifestations in patients with PXDN mutations. The proliferation and differentiation of the lens is disrupted in association with aberrant expression of transcription factor genes (Pax6 and Foxe3) in mutant eyes. Additionally, Pxdn is involved in the consolidation of the basement membrane and lens epithelium adhesion in the ocular lens. Lens material including γ-crystallin is extruded into the anterior and posterior chamber due to local loss of structural integrity of the lens capsule as a secondary damage to the anterior segment development leading to congenital ocular inflammation. Moreover, Pxdn mutants exhibited an early-onset glaucoma and progressive retinal dysgenesis. Transcriptome profiling revealed that peroxidasin affects the transcription of developmental and eye diseases-related genes at early eye development. These findings suggest that peroxidasin is necessary for cell proliferation and differentiation and for basement membrane consolidation during eye development. Our studies provide pathogenic mechanisms of PXDN mutation-induced congenital eye diseases.
2014-05-02 | GSE49704 | GEO
Project description:Temporal transcriptome changes in Drosophila eye development
| PRJNA688743 | ENA
Project description:eyeless (ey) is one of the most critical transcription factors for initiating the entire eye development in Drosophila. However, the molecular mechanisms through which Ey regulates target genes and pathways have not been characterized at the genomic level. Using ChIP-Seq, we generated an endogenous Ey binding profile in Drosophila developing eyes. These data sets will serve as a valuable resource for future studies on Ey and eye development.
2018-09-26 | GSE112868 | GEO
Project description:Analysis of gene expression during Drosophila eye formation. Keywords: other
2003-01-21 | GSE271 | GEO
Project description:Coordinating cell proliferation and differentiation is essential during organogenesis. In Drosophila, the photoreceptor, pigment and support cells of the eye are specified in an orchestrated wave as the morphogenetic furrow passes across the eye imaginal disc. Cells anterior of the furrow are uncommitted to cell type and remain mitotically active, while most cells in the furrow arrest at G1 and adopt specified ommatidial fates. We used microarray expression analysis to monitor changes in transcription at the furrow and identified genes whose expression correlates with either proliferation or fate specification.
2008-09-23 | GSE12851 | GEO
Project description:Impaired GSH biosynthesis disrupts eye development and PAX6 function
| PRJNA732284 | ENA
Project description:Microphthalmos is a rare congenital anomaly characterized by reduced eye size and visual deficits of variable degrees. Sporadic and hereditary microphthalmos has been associated to heterozygous mutations in genes fundamental for eye development. Yet, many cases are idiopathic or await the identification of molecular causes. Here we show that haploinsufficiency of Meis1, a transcription factor with an evolutionary conserved expression in the embryonic trunk, brain and sensory organs, including the eye, causes microphthalmic traits and visual impairment, in adult mice. In the trunk, Meis1 acts as a cofactor for genes of the Hox complex, mostly binding to Hox-Pbx target sequence on the DNA. By combining the analysis of Meis1 loss-of-function and conditional Meis1 functional rescue with ChIPseq and RNAseq approaches, we show that during the development of the optic cup, an Hox-free region, Meis1 binds instead to Hox/Pbx-independent Meis binding site, and coordinates, in a dose-dependent manner, retinal proliferation and differentiation by regulating the expression of components of the Notch signalling pathway. Meis1 also controls the activity of genes responsible for human microphthalmia and eye patterning so that in Meis1-/- embryos, the eye size is reduced and boundaries among the different eye territories are shifted or blurred. We thus propose that Meis1 is at the core of a genetic network implicated in microphthalmia, itself representing an additional candidate for syndromic cases of these ocular malformations. Transcriptomics and Meis1 Occupancy analysis on mouse isolated optic cups and ChIP data for histone methylation marks were obtained from about 100 eyes of E10.5 CD1 embryos.
2015-08-27 | E-GEOD-62786 | biostudies-arrayexpress