RNA-sequencing of mouse adult hippocampal progenitor cells in which Nfix was deleted.
Ontology highlight
ABSTRACT:
ORGANISM(S): Mus musculus
PROVIDER: GSE109817 | GEO | 2018/01/30
REPOSITORIES: GEO
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Project description:RNA-sequencing of mouse adult hippocampal progenitor cells in which Nfix was deleted.
| PRJNA432080 | ENA
Project description:Hematopoietic stem cells are both necessary and sufficient to sustain the complete blood system of vertebrates. Here we show that Nfix, a member of the nuclear factor I (Nfi) family of transcription factors, is highly expressed by hematopoietic stem and progenitor cells (HSPC) of murine adult bone marrow. Although shRNA mediated knockdown of Nfix expression in Lineage-Sca-1+c-Kit+ HSPC had no effect on in vitro cell growth or viability, Nfix-depleted HSPC displayed a significant loss of colony forming potential, as well as short- and long-term in vivo hematopoietic repopulating activity. Analysis of recipient mice 4-20 days post-transplant revealed that Nfix-depleted HSPC establish in the bone marrow but fail to persist due to increased apoptotic cell death. Gene expression profiling of Nfix-depleted HSPC reveals that loss of Nfix expression in HSPC is concomitant with a decrease in the expression of multiple genes known to be important for HSPC survival, such as Erg, Mecom, Mpl and Prdm16. These data reveal that Nfix is a novel regulator of HSPC survival post-transplantation and establish, for the first time, a role for Nfi genes in the regulation of this cellular compartment. 3 NFIX depleted samples are compared to 3 wt samples
2013-09-05 | E-GEOD-45492 | biostudies-arrayexpress
Project description:The generation of cellular identity and diversity within the developing spinal cord is critically dependent on networks of gene expression controlled by transcription factors, such as Nuclear Factor One X (NFIX). NFIX has been identified as an important factor in promoting astrocyte formation during embryonic mouse spinal cord development. To gain a more comprehensive understanding of the transcriptional landscape controlled by NFIX within the developing spinal cord, here we performed microarray analysis on E14.5 wild-type and Nfix-/- mouse spinal cords, the age at which the expression of NFIX by neural progenitor cells lining the spinal central canal is strongest.
2020-07-30 | GSE155327 | GEO
Project description:Hematopoietic stem cells are both necessary and sufficient to sustain the complete blood system of vertebrates. Here we show that Nfix, a member of the nuclear factor I (Nfi) family of transcription factors, is highly expressed by hematopoietic stem and progenitor cells (HSPC) of murine adult bone marrow. Although shRNA mediated knockdown of Nfix expression in Lineage-Sca-1+c-Kit+ HSPC had no effect on in vitro cell growth or viability, Nfix-depleted HSPC displayed a significant loss of colony forming potential, as well as short- and long-term in vivo hematopoietic repopulating activity. Analysis of recipient mice 4-20 days post-transplant revealed that Nfix-depleted HSPC establish in the bone marrow but fail to persist due to increased apoptotic cell death. Gene expression profiling of Nfix-depleted HSPC reveals that loss of Nfix expression in HSPC is concomitant with a decrease in the expression of multiple genes known to be important for HSPC survival, such as Erg, Mecom, Mpl and Prdm16. These data reveal that Nfix is a novel regulator of HSPC survival post-transplantation and establish, for the first time, a role for Nfi genes in the regulation of this cellular compartment.
2013-09-05 | GSE45492 | GEO
Project description:Transcriptional regulation plays a central role in controlling neural stem and progenitor cell proliferation and differentiation during neurogenesis. For instance, transcription factors from the nuclear factor I (NFI) family have been shown to co-ordinate neural stem and progenitor cell differentiation within multiple regions of the embryonic nervous system, including the neocortex, hippocampus, spinal cord and cerebellum. Knockout of individual Nfi genes culminates in similar phenotypes, suggestive of common target genes for these transcription factors. However, whether or not the NFI family regulates common suites of genes remains poorly defined. Here, we use granule neuron precursors (GNPs) of the postnatal murine cerebellum as a model system to analyse regulatory targets of three members of the NFI family: NFIA, NFIB and NFIX. By integrating transcriptomic profiling (RNA-seq) of Nfia- and Nfix-deficient GNPs with epigenomic profiling (ChIP-seq against NFIA, NFIB and NFIX, and DNase I hypersensitivity assays), we reveal that these transcription factors share a large set of potential transcriptional targets, suggestive of complementary roles for these NFI family members in promoting neural development.
2020-03-12 | GSE146793 | GEO
Project description:Overexpressed either GFP, wild-type (WT) NFIX or a phospho-dead mutant of NFIX in which eight serine residues surrounding S286 were mutated to alanine (S265/267/268/271/272/273/274/275A) was performed C2C12 cells prior to the induction of myogenesis. Cells were harvest 2 days post induction of myogensis with 2% horse serum.
2022-05-18 | PXD028718 | Pride
Project description:Human doublecortin (DCX) mutations are associated with severe brain malformations leading to aberrant neuron positioning (heterotopia), intellectual disability and epilepsy. DCX is a microtubule-associated protein which plays a key role during neurodevelopment in neuronal migration and differentiation. Dcx knockout (KO) mice show disorganized hippocampal pyramidal neurons. The CA2/CA3 pyramidal cell layer is present as two abnormal layers and disorganized CA3 KO pyramidal neurons are also more excitable than wild-type (WT) cells. To further identify abnormalities, we characterized Dcx KO hippocampal neurons at subcellular, molecular and ultrastructural levels. Severe defects were observed in mitochondria, affecting number and distribution. Also, the Golgi apparatus was visibly abnormal, increased in volume and abnormally organized. Transcriptome analyses from laser microdissected hippocampal tissue at postnatal day 60 (P60) highlighted organelle abnormalities. Ultrastructural studies of CA3 cells performed in P60 (young adult) and > 9 months (mature) tissue showed that organelle defects are persistent throughout life. Locomotor activity and fear conditioning behavior of young and mature adults was also abnormal: KO mice consistently performed less well than WT littermates, with defects becoming more severe with age. Thus, we show that disruption of a neurodevelopmentally-regulated gene can lead to permanent organelle anomalies contributing to abnormal adult behavior
2022-03-29 | GSE185031 | GEO
Project description:Adult hippocampal neurogenesis (AHN) has been extensively characterized in rodent models, but its existence in humans remains controversial. We sought to assess the phenomenon in post-mortem human hippocampal samples by combining spatial transcriptomics and fluorescent in situ hybridization. We detected very few cells expressing neural stem cell- and proliferation-specific genes in the human dentate gyrus (DG) from childhood to middle age, suggesting very low levels of hippocampal neurogenesis throughout life. However, we observed at all ages a significant number of DG cells expressing the immature neuronal marker DCX. The majority of DCX+ cells displayed an inhibitory phenotype, while the remainder were non-committed or excitatory in nature. Overall, our study investigates for the first time the extent of AHN in the human brain with spatial transcriptomic tools and reveals important insight into the distribution and phenotype of cells expressing neurogenesis markers in the adult human hippocampus.
2024-10-16 | GSE248545 | GEO
Project description:Purpose: To study the mechanisms involved in the regulation by NFIX on neural stem cell development and to examine the transcriptome changes associated with the loss of NFIX in neural stem cells. Methods: Subventricular zones of 10-day-old wild-type and Nfix KO mice were sectioned and dissociated into single cells. Cells were cultured in proliferation condition for 10 days. RNA was purified and poly-A selected to build the library for RNA-seq. Conclusions: Our study represents the first detailed analysis of transcriptome changes in primary monolayer-cultured neural stem cells associated with the loss of NFIX. Cells dissociated from 10-day-old wild-type and nuclear factor I-X (Nfix KO) mice subventricular zone were cultured in DMEM/F12 with B27, Glutamine, EGF and bFGF for 10 days. RNA was harvested with Norgen RNA purification micro kit and then prepared with illumina TruSeq kit. Samples from 6 mice (3 vs. 3) were loaded on one lane. 50-cycle single-read run was performed on Hiseq 2000. The sequence reads were analyzed by TopHat 2.0.7 followed by Cufflinks 1.3.0 with the mm9 UCSC annotation files.
2015-06-30 | E-GEOD-65337 | biostudies-arrayexpress
Project description:Tissue-specific deletion of the gene encoding the histone acetyltransferase Kat7 (Hbo1) in the developing mouse central nervous system using cre-recombinase expression driven by regulatory sequences of the nestin locus (NesCre transgene) resulted in defective cerebral cortex development, a complete failure of neural stem cells to give rise to neurons and oligodendrocytes during in vitro differentiation, and a failure to express the neuronal differentiation program. Proliferating neural stem and progenitor cells (NPSCs) were isolated from Kat7-deleted and Kat7-intact 14.5 day embryonic mouse fetuses.
2022-12-09 | GSE220498 | GEO