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Cell autonomous roles for AP-2alpha in lens vesicle separation and maintenance of the lens epithelial cell phenotype.

ABSTRACT: This is a comparative microarray analysis of LE-AP-2a mutants vs. wild-type P0 littermate lenses. This analysis revealed differential gene expression of 415 mRNAs, including reduced expression of genes important for maintaining lens epithelial cell phenotype, such as E-cadherin. Keywords: Differential gene expression

ORGANISM(S): Mus musculus

PROVIDER: GSE14536 | GEO | 2009/01/24

SECONDARY ACCESSION(S): PRJNA111619

REPOSITORIES: GEO

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Transcription profiling of mouse LE-AP-2a mutants vs. wild-type P0 littermate lenses to investigate cell autonomous roles for AP-2alpha in lens vesicle separation and maintenance of the lens epithelial cell phenotype.

Project description:This is a comparative microarray analysis of LE-AP-2a mutants vs. wild-type P0 littermate lenses. This analysis revealed differential gene expression of 415 mRNAs, including reduced expression of genes important for maintaining lens epithelial cell phenotype, such as E-cadherin. Experiment Overall Design: Biological triplicates of mouse lenses were analyzed (three wild-type lens samples and three Le-AP-2 mutant samples)

2009-01-31 | E-GEOD-14536 | biostudies-arrayexpress

HSF4 microarray gene expression analysis in the newborn mouse lens.

Project description:Differential expression of HSF4 in null newborn mouse and wildtype lenses was examined to identify putative downstream targets of HSF4. To examine roles of Brg1 in mouse lens development, a dnBrg1 transgenic construct was expressed using the lens-specific aA-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 IIb, 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. Keywords: Differential mRNA Expression Three biological replicate experiments were performed with HSF null and wildtype lenses.

2010-12-01 | E-GEOD-22362 | biostudies-arrayexpress

Cell autonomous roles for AP-2alpha in lens vesicle separation and maintenance of the lens epithelial cell phenotype.

Project description: Not available

| S-EPMC2517426 | biostudies-literature

HSF4 microarray gene expression analysis in the newborn mouse lens.

2010-12-01 | GSE22362 | GEO

Chromatin remodeling enzyme Brg1 is required for mouse lens fiber cell terminal differentiation and their denucleation [lens tissue]

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

Chromatin remodeling enzyme Brg1 is required for mouse lens fiber cell terminal differentiation and their denucleation [lens tissue]

2011-01-01 | GSE22322 | GEO

Chromatin remodeling enzyme Brg1 is required for mouse lens fiber cell terminal differentiation and their denucleation [eyeball tissue]

Project description:Genome-wide approach to identify the cell-autonomous role of Brg1 in lens fiber cell terminal differentiation. Differential gene expression was analyzed in Brg1 lens-conditional knockout and wildtype newborn mouse eyeballs, with subsequent comparison of this data with the dnBrg1 mouse lenses expression data. Keywords: Differential gene expression Three biological replicate experiments were performed.

2011-01-01 | E-GEOD-25168 | biostudies-arrayexpress

High-throughput transcriptomics of Celf1 conditional knockout lens identifies downstream networks linked to cataract pathology

Project description:Celf1 germline or conditional deletion mouse mutants exhibit fully penetrant lens defects including cataract. To gain insight into gene expression changes underlying these lens defects Differential Gene Expression analysis was performed for lenses obtained from control and Celf1 conditional deletion mutant mice.

2023-03-18 | GSE227293 | GEO

Chromatin remodeling enzyme Brg1 is required for mouse lens fiber cell terminal differentiation and their denucleation [eyeball tissue]

2011-01-01 | GSE25168 | GEO

Crim1 regulates integrin signaling in murine lens development

Project description:The developing lens is a powerful system for investigating the molecular basis of inductive tissue interactions and for studying cataract, the leading cause of blindness. The formation of tightly controlled cell-cell adhesions and cell-matrix junctions between lens epithelial (LE) cells, between lens fiber (LF) cells, and between these two cell populations enables the vertebrate lens to adopt a highly ordered structure and acquire optical transparency. Adhesion molecules are thought to maintain this ordered structure, but little is known about their identity or interactions. Cysteine-rich motor neuron 1 (Crim1), a type I transmembrane protein, is strongly expressed in the developing lens and its mutation causes ocular disease in both mice and humans. How Crim1 regulates lens morphogenesis is not understood. We identified a novel ENU-induced hypomorphic allele of Crim1, Crim1-glcr11, which in the homozygous state causes cataract and microphthalmia. Using this and two other mutant alleles, Crim1-null and Crim1-cko, we show that the lens defects in Crim1 mouse mutants originate from defective LE cell polarity, proliferation and cell adhesion. Crim1 adhesive function is likely to be required for interactions both between LE cells and between LE and LF cells. We show that Crim1 acts in LE cells, where it colocalizes with and regulates the levels of active β1 integrin and of phosphorylated FAK and ERK. The RGD and transmembrane motifs of Crim1 are required for regulating FAK phosphorylation. These results identify an important function for Crim1 in the regulation of integrin- and FAK-mediated LE cell adhesion during lens development.

2016-12-21 | GSE62561 | GEO

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