Transcriptome of Dmrt3 KO, Dmrt5 KO, Dmrt3;Dmrt5 double KO and wildtype cortical tissue at E12.5.
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ABSTRACT:
ORGANISM(S): Mus musculus
PROVIDER: GSE108611 | GEO | 2018/12/28
REPOSITORIES: GEO
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Project description:Transcriptome of Dmrt3 KO, Dmrt5 KO, Dmrt3;Dmrt5 double KO and wildtype cortical tissue at E12.5.
| PRJNA427815 | ENA
Project description:We then examined the mutant mice that lack both Dmrt3 and Dmrta2 alleles, and found the size of the medial cortex including the hippocampus and the cortical hem was significantly reduced in mutant brains .To further investigate how Dmrt3 and Dmrta2 are involved in the development of the medial cortex, we applied gene expression profiling approach using whole genome DNA microarray to identify genes which are differentially expressed in Dmrt3/Dmrta2-knockdown cells. Cortical cells knocked-down both Dmrt3 and Dmrta2 exhibited a dramatic increase of Pax6 expression in the medial cortex, leading to the precocious neuronal differentiation, and simultaneous knockdown of Pax6 with Dmrt3/Dmrta2 rescued the phenotype. Our results unveil a key mechanism that mammalian Dmrt factors maintain more proliferative potential of neural progenitors by suppressing Pax6 expression in the developing cerebral cortex.
2019-08-03 | GSE83639 | GEO
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: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:Increased cortical size is essential to the enhanced intellectual capacity of primates during mammalian evolution. The mechanisms that control cortical size are largely unknown. Here, we show that mammalian BAF170, a subunit of the chromatin remodeling complex mSWI/SNF, is an intrinsic factor that controls cortical size. We find that the conditional deletion of BAF170 promotes indirect neurogenesis by increasing the pool of intermediate progenitors (IPs) and results in an enlarged cortex, whereas cortex-specific BAF170 over-expression results an opposing phenotype. Mechanistically, BAF170 competes with BAF155 subunit in the BAF complex, affecting the euchromatin structure and thereby modulating the binding efficiency of Pax6/REST-corepressor complex to Pax6 target genes that regulate the generation of IPs and late cortical progenitors. Our findings reveal a molecular mechanism mediated by the mSWI/SNF chromatin-remodeling complex that controls cortical architecture. Cortical gene expression is compared between three E12.5 mouse embryos with cortex-specific loss of BAF170 function and three littermate control embryos.
2013-05-02 | E-GEOD-45629 | biostudies-arrayexpress
Project description:Purpose:To asses changes in gene expression profiles of single cell from the E16.5 wild type littermate controls cortex, and ShhN IUE (ShhN palsmid were electroporated to wild type mice cortex at E13.5 and the cortex were dissected at E16.5) mice. Methords: E16.5 wild type and ShhN-IUE cortices were carefully dissected under a fluorescent stereoscope, and incubated in 4 ml of papain solution for 20 min at 37℃, The cortical tissues were gently triturated, filtered through a 40 mm strainer, and washed with HBSS to obtain the single cell suspension. The Chromium droplet-based sequencing platform (10X Genomics) was used to generate scRNA-seq libraries, following the manufacturer’s instructions. The cDNA libraries were purified, quantified using Agilent 2100 Bioanalyzer, and sequenced on the Illumina Hiseq4000 Results: 7834 cells (2368 median genes per cell) captured for the Control cortex. And 8538 cells with 2422 median genes per cell captured for Shh-IUE mice.
2020-02-19 | GSE140816 | GEO
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:Purpose:To asses changes in gene expression profiles of single cell from the E39 Ferret Cortex. Mouse E18 littermate controls cortex, and Smo CKO (SmoF/F hGFAP-Cre) mice. Methords: E39 ferret cortex, E18 wild type and Smo CKO cortices were carefully dissected under a fluorescent stereoscope, and incubated in 4 ml of papain solution for 20 min at 37℃, The cortical tissues were gently triturated, filtered through a 40 mm strainer, and washed with HBSS to obtain the single cell suspension. The Chromium droplet-based sequencing platform (10X Genomics) was used to generate scRNA-seq libraries, following the manufacturer’s instructions. The cDNA libraries were purified, quantified using Agilent 2100 Bioanalyzer, and sequenced on the Illumina Hiseq4000 Results: E18 SmoF/F (control) cortex, 10524 cells, 1954 genes/cell; hGFAP-Cre; SmoF/F cortex, 7596 cells, 2104 genes/cell; E39 ferret cortex, 23482 cells, 1759 genes/cell.
2023-06-12 | GSE221389 | GEO
Project description:Gene expression analysis of 2-month-old APP/APLP2 double-conditional Knockout (N-dCKO) mice and littermate APLP2 knockout controls, APP knockout and wildtype controls. Mouse hippocampus were dissected for RNA extraction and hybridization on Affymetrix microarrays.
2013-07-10 | E-GEOD-48622 | biostudies-arrayexpress
Project description:Modeling Focal Cortical Dysplasia (FCD) using cortical organoids
| PRJNA730718 | ENA