RNA-Seq analysis of E15.5 mouse Insm1, Neurod1 and Pax6 knockouts vs Insm1GFP.Cre/+ controls
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PROVIDER: PRJEB43866 | ENA |
REPOSITORIES: ENA
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Project description:This experiment used RNA-Seq technology to explore gene expression in mouse Insm1GFP.Cre/+ controls and Insm1 (Insm1GFP.Cre/GFP.Cre), Neurod1 (Insm1GFP.Cre/+; Neurod1LacZ/LacZ), or Pax6 (Insm1GFP.Cre/+; Pax6fl/fl) knockout FACS sorted pancreatic endocrine cells at E15.5. Comparison of Insm1GFP.Cre+/- and knockout animals revealed sets of differentially expressed genes that are required for endocrine cell specification and development.
2021-08-23 | E-MTAB-10262 | biostudies-arrayexpress
Project description:Genome-wide Insm1 binding sites analysis revealed an overrepresentation of sequences predicted to bind bHLH and/or forkhead factors, and further analyses demonstrated that most Insm1 sites in the genome are co-occupied by Neurod1 and Foxa2. Binding regions co-occupied by all three factors but not single Insm1 sites explained a significant fraction of gene expression changes in Insm1 mutant β-cells. Together, our data provide evidence that an Insm1, Neurod1 and Foxa2 network maintains a mature gene expression program in β-cells. 6 samples include, replicates of Insm1 and Foxa2, IgG pull down as a control
2015-03-31 | E-GEOD-54046 | biostudies-arrayexpress
Project description:Genome-wide Insm1 binding sites analysis revealed an overrepresentation of sequences predicted to bind bHLH and/or forkhead factors, and further analyses demonstrated that most Insm1 sites in the genome are co-occupied by Neurod1 and Foxa2. Binding regions co-occupied by all three factors but not single Insm1 sites explained a significant fraction of gene expression changes in Insm1 mutant β-cells. Together, our data provide evidence that an Insm1, Neurod1 and Foxa2 network maintains a mature gene expression program in β-cells.
2015-03-31 | GSE54046 | GEO
Project description:Pax6 is a transcription factor with key functional roles in embryonic development. In order to identify downstream effectors of Pax6 in the developing cerebral cortex we performed microarray analysis. We compared gene expression profiles of cortical tissues isolated from wild type and Pax6-/- mouse embryos.
2011-10-31 | GSE32271 | GEO
Project description:Pax6 is a transcription factor with key functional roles in embryonic development. In order to identify downstream effectors of Pax6 in the developing cerebral cortex we performed microarray analysis. We compared gene expression profiles of cortical tissues isolated from wild type and Pax6-/- mouse embryos. In order to identify Pax6 downstream targets we carried out microarray analysis of Pax6-/- mutant mice. Pax6 is highly expressed in the mouse cerebral cortex at embryonic day E14.5, therefore we selected this tissue in order to compare gene expression profiles between wild type and Pax6-/- homozygous cortici. RNA samples were isolated from three mutant and three wild type embryos.
2011-10-31 | E-GEOD-32271 | biostudies-arrayexpress
Project description:The mechanisms by which the early spatiotemporal expression patterns of transcription factors such as Pax6 regulate the region-specific proliferation rates of neural progenitors are poorly understood. Pax6 is expressed in a gradient across the developing cortex and is essential for normal corticogenesis. We found that constitutive or conditional loss of Pax6 increases cortical progenitor proliferation by amounts that vary regionally with normal Pax6 levels. We compared the gene expression profiles of equivalent Pax6-expressing progenitors isolated from Pax6+/+ and Pax6-/- cortices and identified many negatively-regulated cell cycle genes including those encoding Cyclins and Cdks. Biochemical assays indicated that Pax6 directly represses Cdk6 expression. Cyclin/Cdk repression inhibits retinoblastoma protein (pRb) phosphorylation, thereby limiting the transcription of genes directly promoting mitosis, and we showed that Pax6 inhibits pRb phosphorylation and represses several genes involved in DNA replication. Our results indicate that Pax6’s modulation of the cell cycles of cortical progenitors is regional and direct.
2013-01-31 | GSE38703 | GEO
Project description:During organogenesis, PAX6 is required for establishment of various progenitor subtypes within the central nervous system, eye and pancreas. PAX6 expression is maintained in a variety of cell types within each organ, although its role in each lineage and how it acquires cell-specific activity remain elusive. Herein, we aimed to determine the roles and the hierarchical organization of the PAX6-dependent gene regulatory network during the differentiation of the retinal pigmented epithelium (RPE). Somatic mutagenesis of Pax6 in the differentiating RPE revealed that PAX6 functions in a feed-forward regulatory loop with MITF during onset of melanogenesis. PAX6 both controls the expression of an RPE isoform of Mitf and synergizes with MITF to activate expression of genes involved in pigment biogenesis. This study exemplifies how one kernel gene pivotal in organ formation accomplishes a lineage-specific role during terminal differentiation of a single lineage. The data contains 3 control and 3 Pax6 negative samples representing biological repeats. Each sample was prepared from RPE dissected from E15.5 transgenic animals, either Pax6loxP/loxP or Pax6loxP/loxP;DctCre.
2014-04-08 | E-GEOD-56548 | biostudies-arrayexpress
Project description:The mechanisms by which the early spatiotemporal expression patterns of transcription factors such as Pax6 regulate the region-specific proliferation rates of neural progenitors are poorly understood. Pax6 is expressed in a gradient across the developing cortex and is essential for normal corticogenesis. We found that constitutive or conditional loss of Pax6 increases cortical progenitor proliferation by amounts that vary regionally with normal Pax6 levels. We compared the gene expression profiles of equivalent Pax6-expressing progenitors isolated from Pax6+/+ and Pax6-/- cortices and identified many negatively-regulated cell cycle genes including those encoding Cyclins and Cdks. Biochemical assays indicated that Pax6 directly represses Cdk6 expression. Cyclin/Cdk repression inhibits retinoblastoma protein (pRb) phosphorylation, thereby limiting the transcription of genes directly promoting mitosis, and we showed that Pax6 inhibits pRb phosphorylation and represses several genes involved in DNA replication. Our results indicate that Pax6M-bM-^@M-^Ys modulation of the cell cycles of cortical progenitors is regional and direct. Two condition experiment, Pax6sey/sey vs Pax6+/+ cortical progenitor cells from lateral cortex. 3 biological replicates. Each replicate contains RNA from cells pooled from 4 individual E12.5 embryos
2013-01-31 | E-GEOD-38703 | biostudies-arrayexpress
Project description:This experiment used RNA-Seq technology to explore gene expression in mouse Insm1^GFP/Pdx1^CFP HIGH [het/het] FACS sorted pancreatic cells (pre-beta cells) and Insm1^GFP/Pdx1^CFP LOW [het/het] cells (other endocrine progenitors) at E15.5 and E18.5. Comparison of Insm1 +/Pdx HIGH and Insm1 +/Pdx LOW cells revealed a set of differentially expressed genes that are required for beta cell specification.
2014-07-01 | E-MTAB-1929 | biostudies-arrayexpress
Project description:NeuroD1 encodes a basic helix-loop-helix transcription factor involved in the development of neural and endocrine structures. NeuroD1 mRNA is highly abundant in the adult mammalian pineal gland and exhibits a developmental expression pattern similar to the retina. This is consistent with the common evolutionary origin of pinealocytes and retinal photoreceptors. Pinealocytes and retinal photoreceptors express a shared set of phototransduction genes and submammalian pinealocytes are photosensitive. In contrast to the retina, the pineal gland is a relatively homogeneous structure, composed 95% of pinealocytes. This makes the pineal gland a particularly useful model for understanding photoreceptor cell biology. The loss of NeuroD1 in the retina results in progressive photoreceptor degeneration and the molecular mechanisms underlying this retinal degeneration phenotype remain unknown. Similarly, the role that NeuroD1 plays in the pineal gland is unknown. To determine the function of NeuroD1 in the pineal gland and retina, a Cre/loxP recombination strategy was used to selectively target a NeuroD1 floxed allele and generate NeuroD1 conditional knockout (cKO) mice. Tissue specificity was conferred using Cre recombinase expressed under the control of the promoter of Crx, a transcription factor selectively expressed in the pineal gland and retina. Pineal and retinal tissues from two-month-old NeuroD1 cKO and control animals were used in microarray studies to identify candidate genes responsible for the photoreceptor degeneration phenotype. The Cre/loxP recombination strategy was used to target a NeuroD1 floxed allele and generate NeuroD1 conditional knockout mice (NeuroD1floxed::Crx-Cre+/-). NeuroD1 floxed mice (NeuroD1floxed::Crx-Cre-/-) served as the controls. Pineal glands and retinas from two-month-old control and conditional knockout mice were collected at ZT6 and ZT20. 3 pools of 6 pineal glands per genotype and respective time of day were collected for each sample. Similarly, 3 pools of 6 retinas each were also collected. RNA from each pool was extracted and hybridized on the Affymetrix Mouse 430 2.0 array.
2012-07-25 | E-GEOD-35396 | biostudies-arrayexpress