Mus musculus
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA151063 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Gene expression profiling of mouse cortices in which the experimental strain lacks Exon 6 of the Snf2l gene which encodes an ATP-binding motif that is critical for chromatin re-modeling Comparison of gene expression in E15.5 cortices of Snf2l-Ex6DEL mice versus wild type controls. Two samples of each strain were used, with one pair of samples utilized for two of the replicates (dye-flip), the second pair then used for the third replicate.
2012-04-09 | E-GEOD-34998 | biostudies-arrayexpress
Project description:Purpose:To assess changes in gene expression profiles of single cell from the wild type littermate controls cortices in E13.5, E15.5 and P0, and conditional knockout Bcl11a (and Bcl11b) at cortical projection neurons in the mouse cortices of the same ages. Methods: E13.5, E15.5 and P0 control and mutant cortices were carefully dissected under a clean environment. Then total RNA was isolated using an RNeasy Mini Kit (QIAGEN) according to the manufacturer’s protocol, quantified using NanoDrop ND-2000, and checked for RNA integrity using Agilent 2100 bioanalyzer. RNA-seq libraries were prepared according to the Illumina TruSeq protocol. Results: An average of 15 million reads per sample were obtained.
2021-08-31 | GSE182990 | GEO
Project description:Conditional deletion of Geminin from the entire hematopoietic compartment using Vav1:iCre mice led to defective hematopoiesis/dyserythropoiesis in E15.5 mouse embryos. The present data set includes data from lineage-negative cells isolated from homogenized livers that were dissected from E15.5.dpc embryos. The two conditions compared were wild-type versus Geminin-KO Lin- cells. The cells were collected from littermates.
2015-01-07 | GSE53056 | GEO
Project description:Gene expression profiling of mouse cortices in which the experimental strain lacks Exon 6 of the Snf2l gene which encodes an ATP-binding motif that is critical for chromatin re-modeling
2012-04-10 | GSE34998 | GEO
Project description:Purpose: We applied polyA site sequencing (Passeq) to human Huntington's disease and control motor cortex and cerebellum to test if any genes change 3′UTR isoforms abundance. Methods: 3′ sequencing was performed on 6 motor cortices from grade 1 Huntington's patient brains, 4 motor cortices from grade 2 Huntington's patient brains, and 5 motor cortices from control brains. Cerebellum samples included 9 cerebella from grade 2-3 Huntington's patient brains, and 7 cerebella from control brains. To verify HTT isoforms in mice, sequencing was performed on 5 Q140 mouse striata and 3 wild-type mouse striata. Results: We report 11% of genes from Huntington's disease patient motor cortex exhibit a change in at least one of their 3′UTR isoforms, commensurate with the 11% of genes which show different total expression in HD motor cortex versus control. In contrast, gene isoform and expression changes are minimal (<5%) in Huntington's disease cerebellum versus controls. In the motor cortex, we show isoform and gene expression differs between between grade 1 and grade 2 brains. We identify a novel isoform of huntingtin mRNA which is conserved in wild-type and Huntington's model mice. Conclusions: This is the first study characterizing widespread alterations in 3′UTR isoform abundance in Huntington's disease. Alterations in isoform abundance may affect mRNA metabolism in Huntington's disease brains.
2017-09-21 | GSE96099 | GEO
Project description:Mouse P10 cerebellum: Smarca5 conditional KO mice (cKO) versus wild type controls
| PRJNA181201 | ENA
Project description:Mouse P0 cerebellum: Smarca5 conditional KO mice (cKO) versus wild type controls
| PRJNA181200 | ENA
Project description:Snf2l and the closely related protein, Snf2h, play a critical role in embryonic and post-natal brain development. Murine models lacking functional Snf2h or Snf2l point to complementary activities of these remodelers; Snf2h cKO mice present with a significantly reduced cerebellum, while Snf2l Ex6DEL cerebella are larger than their wild-type counterparts. Granule neuron progenitors (GNPs) isolated from Ex6DEL cerebella display delayed cell cycle exit and hindered terminal differentiation compared to wild-type littermates. Moreover, loss of Snf2l activity results in widespread transcriptome shifts which underlie the Ex6DEL GNP differentiation phenotype. In particular, key transcription factors (TFs) are differentially expressed without Snf2l remodelling activity. We confirm that ERK pathway activation is misregulated in Ex6DEL GNPs, possibly in response to elevated fibroblast growth factor 8 (Fgf8) expression in these cultures. We find that Snf2l activity maintains the chromatin landscape throughout GNP differentiation, as Ex6DEL cultures have a global increase in chromatin accessibility. We suggest that Snf2l-mediated chromatin condensation is responsible for proper regulation of gene expression programs in GNP differentiation.
2019-12-31 | GSE122173 | GEO
Project description:Snf2l and the closely related protein, Snf2h, play a critical role in embryonic and post-natal brain development. Murine models lacking functional Snf2h or Snf2l point to complementary activities of these remodelers; Snf2h cKO mice present with a significantly reduced cerebellum, while Snf2l Ex6DEL cerebella are larger than their wild-type counterparts. Granule neuron progenitors (GNPs) isolated from Ex6DEL cerebella display delayed cell cycle exit and hindered terminal differentiation compared to wild-type littermates. Moreover, loss of Snf2l activity results in widespread transcriptome shifts which underlie the Ex6DEL GNP differentiation phenotype. In particular, key transcription factors (TFs) are differentially expressed without Snf2l remodelling activity. We confirm that ERK pathway activation is misregulated in Ex6DEL GNPs, possibly in response to elevated fibroblast growth factor 8 (Fgf8) expression in these cultures. We find that Snf2l activity maintains the chromatin landscape throughout GNP differentiation, as Ex6DEL cultures have a global increase in chromatin accessibility. We suggest that Snf2l-mediated chromatin condensation is responsible for proper regulation of gene expression programs in GNP differentiation.
2019-12-31 | GSE122172 | GEO