Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Breasi-CRISPR Ccnd2 Thr280Ala mutation E13.5-E15.5 embryonic mouse cortex

ABSTRACT: Breasi-CRISPR Ccnd2 Thr280Ala mutation E13.5-E15.5 embryonic mouse cortex

PROVIDER: PRJNA1051107 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Similar Datasets

Breasi-CRISPR Ccnd2 Thr280Ala mutation E13.5-E15.5 embryonic mouse cortex

Project description:Here we demonstrate the ability to model patient variants associated with two different NDDs in vivo using Breasi-CRISPR. We first model periventricular nodular heterotopia (PVNH), a neuronal migration disorder (Heinzen et al., 2018; Walters et al., 2018). We use Breasi-CRISPR to insert two patient analogous protein truncating variants in MAP1B, resulting in a significant defect in migration. We were able to validate that MAP1B fragments are being produced from these protein truncating variants, but the fragments do not act as a dominant negative. Next, we modeled a patient variant in CCND2 (encoding the protein cyclin D2) associated with megalencephaly postaxial polydactyly polymicrogyria hydrocephalus (MPPH) syndrome (Mirzaa et al., 2014). The unifying pathogenic mechanism underlying MPPH syndrome is believed to be excessive cyclin D2, a cell cycle regulator known to promote cell cycle progression. Modeling the repeated variant Thr280Ala caused an increase in the number of cells in S phase, an increase in progenitor numbers, an accumulation of cyclin D2 protein, and a tangential expansion of the cortex. We wondered if Breasi-CRISPR would be efficient enough to notice transcriptomic changes via bulk RNA sequencing of the targeted area. Indeed, we found that introduction of the MPPH syndrome variant caused an upregulation of genes and pathways important in tissue growth and a downregulation of those important in cell differentiation. Taken together we demonstrate that Breasi-CRISPR is efficient enough to model patient analogous variants, mirroring patient phenotypes and enabling investigation of NDDs.

2024-12-08 | GSE249900 | GEO

Whole transcriptome RNAseq analysis of E13.5, E15.5 and PND 0 Inha WT and KO testes

Project description:We performed bulk RNA-Seq on testes from E13.5, E15.5 and PND 0 whole testes from Inha WT and KO mouse (lacking the inhibin a gene).

2023-08-08 | GSE236618 | GEO

RNAseq comparison of gene expression profiles in ScxGFP positive cells from E11.5, E13.5 and E15.5 hindlimb samples

Project description:RNAs were isolated from FACS sorted ScxGFP positive cells of hindlimbs at E11.5, E13.5 and E15.5, and characterized by RNAseq

2015-03-19 | GSE65179 | GEO

The chromatin accessibility in mouse pancreatic epithelial cells at E11.5, E13.5 and E15.5 during embryogenesis [ATAC-seq]

Project description:To understand the chromatin accessibility in mouse pancreatic epithelial cells at different stages during fetal development, we performed ATAC-seq in epithelial cells sorted from the pancreas tissues of E11.5, E13.5 and E15.5

2023-12-22 | GSE218736 | GEO

Single cell RNA sequencing of fetal mouse intestine at key stages of development (E13.5, E14.5, E15.5, E16 and E17.5)

Project description:Here, we present the fetal mouse intestine data from the project \\"Comparison of human and mouse mesenchyme identifies common and unique aspects of intestinal patterning\\". Whole intestines were harvested from fetuses from timed pregnant matings for wildtype C57BL/6 mice (Jax strain #000664). Fetal stages were confirmed according to the Theiler staging chart (https://www.emouseatlas.org/emap/ema/staging_criteria/staging_criteria.html). Whole intestines (from the common bile duct through the cecum) were collected at key stages of development (E13.5, E14.5, E15.5, E16 and E17.5). Male and female intestines from each stage were pooled and dissociated to single cells for single cell RNA sequencing as previously described (Miller et al. 2020 Dev Cell). Specifically, E13.5 was 6 intestines, E14.5 was 5 intestines, E15.5 was 4 intestines, E16 was 3 intestines and E17.5 was 3 intestines.

2024-04-01 | E-MTAB-13201 | biostudies-arrayexpress

Transcriptome analysis of electroporated/GFP+ cells from embryonic mouse cortex E15.5 (E13.5 + 48 h), shRNA against circSlc45a4, mRNA Slc45a4 and scramble KD

Project description:We perturbed the expression levels of circSlc45a4 and mRNA Slc45a4 in developing mouse cortex (E15.5) by RNAi/shRNAs. 48 h post-electroporation the cells were isolated by FACS (GFP+), RNA was extracted with Trizol and polyA+ libraries were generated with Illumina TruSeq Stranded mRNA LT Sample Prep Kit. We find many significant changes in the transcriptomic profile after knockdown of circSlc45a4 and mRNA Slc45a4, that are distinct from each other.

2019-03-31 | GSE124000 | GEO

Transcriptome analysis of electroporated/GFP+ cells from embryonic mouse cortex E15.5 (E13.5 + 48 h), shRNA against circSlc45a4, mRNA Slc45a4 and scramble KD

Project description:Transcriptome analysis of electroporated/GFP+ cells from embryonic mouse cortex E15.5 (E13.5 + 48 h), shRNA against circSlc45a4, mRNA Slc45a4 and scramble KD

| PRJNA510529 | ENA

Early lineage commitment defines alveolar epithelial ontogeny in the lung (E13.5, E15.5 and E17.5)

Project description:Early lineage commitment defines alveolar epithelial ontogeny in the lung (E13.5, E15.5 and E17.5)

| PRJNA578717 | ENA