Expression in the dorsal telencephalon of E13.5 conditional Dicer KO mice
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ABSTRACT:
ORGANISM(S): Mus musculus
PROVIDER: GSE37610 | GEO | 2012/08/30
SECONDARY ACCESSION(S): PRJNA162285
REPOSITORIES: GEO
Similar Datasets
Project description:To study the effect of miRNA depletion in the embryonic forebrain, we isolated RNA from E13.5 dorsal telencephalon of mice homozygous for a floxed Dicer allele and hemizygous for the forebrain expressed Emx1Cre (Dicer KO mice). These samples were compared to littermates heterozygous for the floxed allele and hemizygous for Emx1Cre. 5 Dicerko mice and 4 controls, partly littermates, no technical replicates
2012-08-30 | E-GEOD-37610 | biostudies-arrayexpress
Project description:Wild type and Dicer null embryonic mouse limbs were analaysed using Affymetrix arrays to identify gene expression changes. Genes that were up-regulated in Dicer-null limbs were canidates for being miRNA targets. Potential miRNA target genes were validated using qRTPCR. Mice carrying a heterozygous Dicer floxed allele and the prxcre driver allele were crossed to homozygous Dicer Floxed mice. Embryos were harvested from pregent moms and genotyped to determine heterozygous, Wild type and mutant limb buds. These limb buds were used to prepare RNA for array analysis.
2011-01-31 | E-GEOD-13807 | biostudies-arrayexpress
Project description:In this study, we wanted to compare CTCF binding sites in whole telencephalon vs medial ganglionic eminence (MGE) at embryonic day E13.5.
2019-04-05 | GSE105071 | GEO
Project description:The mammalian telencephalon plays critical roles in cognition, motor function, and emotion. While many of the genes required for its development have been identified, the distant‐acting regulatory sequences orchestrating their in vivo expression are mostly unknown. Here we describe a digital atlas of in vivo enhancers active in subregions of the developing telencephalon. We identified over 4,600 candidate embryonic forebrain enhancers and studied the in vivo activity of 329 of these sequences in transgenic mouse embryos. We generated serial sets of histological brain sections for 145 reproducible forebrain enhancers, resulting in a publicly accessible web‐based enhancer atlas comprising over 33,000 sections. We show how this large collection of annotated telencephalon enhancers can be used to study the regulatory architecture of individual genes, to examine the sequence motif content of enhancers, and to drive targeted reporter or effector protein expression in experimental applications. Furthermore, we used epigenomic analysis of human and mouse cortex tissue to directly compare the genome‐wide enhancer architecture in these species. This atlas provides a primary resource for investigating gene regulatory mechanisms of telencephalon development and enables studies of the role of distant‐acting enhancers in neurodevelopmental disorders. Examination of p300 binding in mouse embryonic stage 11.5 forebrain, mouse postnatal (P0) cortex tissue and human fetal (gestational week 20) cortex
2013-01-29 | E-GEOD-42881 | biostudies-arrayexpress
Project description:The mammalian telencephalon plays critical roles in cognition, motor function, and emotion. While many of the genes required for its development have been identified, the distant‐acting regulatory sequences orchestrating their in vivo expression are mostly unknown. Here we describe a digital atlas of in vivo enhancers active in subregions of the developing telencephalon. We identified over 4,600 candidate embryonic forebrain enhancers and studied the in vivo activity of 329 of these sequences in transgenic mouse embryos. We generated serial sets of histological brain sections for 145 reproducible forebrain enhancers, resulting in a publicly accessible web‐based enhancer atlas comprising over 33,000 sections. We show how this large collection of annotated telencephalon enhancers can be used to study the regulatory architecture of individual genes, to examine the sequence motif content of enhancers, and to drive targeted reporter or effector protein expression in experimental applications. Furthermore, we used epigenomic analysis of human and mouse cortex tissue to directly compare the genome‐wide enhancer architecture in these species. This atlas provides a primary resource for investigating gene regulatory mechanisms of telencephalon development and enables studies of the role of distant‐acting enhancers in neurodevelopmental disorders.
2013-01-29 | GSE42881 | GEO
Project description:The RNase III enzyme dicer is essential for the processing of microRNAs (miRNAs) and small interfering RNAs (siRNAs) from double-stranded RNA precursors. miRNAs and siRNAs regulate chromatin structure, gene transcription, mRNA stability and translation in a wide range of organisms. To provide a model system to explore the role of dicer-generated RNAs in the differentiation of mammalian cells in vivo, we have generated a conditional dicer allele. Deletion of dicer at an early stage of T cell development compromised the survival of αβ lineage cells, while the numbers of γδ-expressing thymocytes were not affected. In developing thymocytes, dicer was not required for the maintenance of transcriptional silencing at pericentromeric satellite sequences (constitutive heterochromatin), the maintenance of cytosine DNA methylation and X chromosome inactivation in female cells (facultative heterochromatin) and the stable shutdown of a developmentally regulated gene (developmentally regulated gene silencing). Most remarkably, given that one-third of mammalian mRNAs are putative miRNA targets, dicer appears to be dispensable for CD4/8 lineage commitment, a process where epigenetic regulation of lineage choice has been well documented. Thus, although dicer appears critical for the development of the early embryo, it may have limited impact on the implementation of lineage-specific gene expression programs. LckCre was used to delete a floxed Dicer1 allele from developing thymocytes (Cobb BS, Nesterova TB, Thompson E, Hertweck A, O'Connor E, Godwin J, Wilson CB, Brockdorff N, Fisher AG, Smale ST and Merkenschlager M. T cell lineage choice and differentiation in the absence of the RNAse III enzyme dicer. J. Exp. Med. 2005 201: 1367-1373). Thymocytes were stained for CD4 and CD8, and double-positive (DP) thymocytes were sorted by flow cytometry. Three biological replicates of Dicer lox/lox control samples and LckCre Dicer lox/lox KO samples were analysed.
2015-01-28 | E-GEOD-57511 | biostudies-arrayexpress
Project description:Background & Aims: MiRNAs are small (~22 nucleotide), non-coding RNA molecules that regulate gene expression through imperfect complementarity with target messenger RNAs. The function of miRNA in mammalian organogenesis is largely unknown. Conditional loss-of-function of Dicer, the enzyme that processes precursor miRNA transcripts into their mature, active form, has been shown to cause severe defects in a number of organ systems. Here we address the role of Dicer in liver development and function. Methods: Mice lacking Dicer function in hepatocytes were generated using an Afp-Cre strain to drive deletion of a floxed Dicer allele. Deletion of the flox-dicer allele was confirmed by quantitative PCR. Decreased miRNA levels detected by quantitative RT-PCR and in situ hybridization confirmed loss of Dicer function. Gene expression microarray analysis was performed on liver RNA from P28 mutant and control mice. Liver sections from mutant and control mice ranging from embryonic stages through 3-4 months of age were examined and liver function tests were performed on adult mice. Results: Mice lacking hepatocyte Dicer function were born alive at the expected frequency, and had grossly normal appearance and behavior. Despite the loss of mature miRNA, hepatic function was normal, as reflected by normal blood gludose, albumin, cholesterol, and bilirubin. However, mutant mice between 2-4 months of age exhibit progressive hepatocyte damage, elevated ALT/AST, with evidence of balanced proliferation and apoptosis in the lobule. Microarray analysis indicates large-scale changes in gene expression, with increased expression of many miRNA targets, as well as imprinted genes. Conclusions: Loss of miRNA processing in the liver at late gestation has a remarkably mild phenotype, suggesting that miRNAs do not play an essential role in hepatic physiology. However, miRNA deficiency results in hepatocyte apoptosis and balanced hepatocyte regeneration. Finally, microarray analysis of gene expression in mutant liver suggests a previously unrecognized role for Dicer in the repression of imprinted genes. Keywords: Genetic modification
2008-12-31 | GSE11899 | GEO
Project description:The precise mechanisms by which microRNAs (miRNAs) contribute to the dynamic regulation of gene expression during forebrain development are still partly elusive. Here we show that depletion of miRNAs via genetic inactivation of Dicer after the onset of forebrain neurogenesis profoundly impairs the morphological and proliferative characteristics of neural stem and progenitor cells.
2012-11-14 | E-MTAB-1062 | biostudies-arrayexpress
Project description:Expression in the dorsal telencephalon of E13.5 conditional Dicer KO mice
| PRJNA162285 | ENA