Expression data from control or Hnf6/Oc2 compound mutant mouse embryonic spinal cords
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA483468 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:In the embryonic spinal cord, cardinal populations of interneurons (INs) diversify into specialized subsets and migrate to defined locations within the spinal parenchyma.However, the factors that control IN diversification and migration remain almost totally unknown. We demonstrate with that Onecut proteins regulate the diversification and the migration of V2 INs in the spinal parenchyma. To identify genes downstream of Onecut transcription factors that may contribute to V2 interneuron differentiation and distribution, we performed a microarray comparison of control and of OC-deficient spinal cord transcriptome at e11.5, namely at the stage when significant numbers of V2 cells have been generated and are initiating migration
2018-07-31 | GSE117871 | GEO
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:Experimental autoimmune encephalomyelitis (EAE) is a mouse model for multiple sclerosis (MS) a chronic autoimmune disease of the central nervous system. We have observed dysfunction of the RNA binding protein hnRNP A1 in neurons from the brains of patients with MS, and the spinal cords of mice with EAE. Here, we sought to characterize the consequences of EAE-induced dysfunction of hnRNP A1 on the RNAs it binds by using CLIPseq to establish both the normal central nervous system RNA binding profile of hnRNP A1 in the spinal cords of naive mice, and any alterations to the binding profile of hnRNP A1 in the spinal cords of mice with EAE.
2024-01-04 | GSE208093 | GEO
Project description:We prepared spinal cords from SOD1-G93A and WT mice treated with vehicle or the RIPK1 inhibitor Nec-1s, which were single cell RNA sequenced using the DropSeq protocol.
2021-03-24 | GSE167198 | GEO
Project description:The goal of this study is to elucidate the influence of treadmill training on transcriptome of the upper lumbar spinal cord after thoracic spinal cord hemisection. mRNA profiles of spinal cords at 23 days-post injury with/without treadmill training were generated. The expression levels of 650 genes in the trained animal were increased ( > 2-fold) compared to untrained animals. Our study represents the detailed analysis of transcriptomes of spinal cord distal to the hemisected lesion after treadmill training, with biologic replicates, generated by RNA-seq technology.
2019-01-15 | GSE115156 | GEO
Project description:We compare transcriptomic profiles of human induced pluripotent stem cells (iPSCs), motor neurons (MNs) in vitro differentiated from iPSCs or human ESCs containing a HB9::GFP reporter for MNs, and human fetal spinal cords. The purpose of this comparison is to assess the extent of molecular similarities between in vitro differentiated MNs and in vivo fetal or adult spinal cord MNs. Data for adult spinal cord MNs are published from other studies: GSE3526, GSE19332, GSE20589, and GSE40438. Human induced pluripotent stem cells, pluripotent stem cell derived motor neurons, and fetal spinal cords for RNA extraction and hybridization on Affymetrix arrays.
2016-06-26 | E-GEOD-75701 | biostudies-arrayexpress
Project description:This laboratory works on selectins and their carbohydrate ligands in lymphocyte homing and inflammation. The lab also studies heparin-degrading endosulfatases and their roles in regulating the interactions of growth factors and morphogens with proteoglycans. The purpose of the experiment is to examine gene expression profiles in spinal cords of injured as a function of time after a contusion injury. The tissue will be generated in the lab of Linda Noble, Professor in the Department of Neurological Surgery at UCSF who is an expert on the pathogenesis of spinal cord injury. Wild-type male C57B/6 mice (8-10 weeks of age) were used. Injuries were produced by contusion. Spinal cords from control mice (uninjured) and experimental (injured) mice were processed (4 and 7 days after injury). A 3 mm length of spinal cord (centered at the injury) and a 3 mm segment from a distant site were isolated from each animal. Tissue from 3 mice were pooled for each sample. Three replicate samples per treatment group were processed for RNA. Thus, a total of 18 RNA samples were hybridized to 18 gene chips. The analysis will determine whether specific glycosylation changes accompany spinal cord injury. Of particular interest are changes in the sulfation profile of proteoglycan GAG chains (e.g., chondroitin sulfate) and in the appearance of potential carbohydrate ligands for infiltrating leukocytes bearing L-selectin or other endogenous lectins.
2011-02-17 | E-GEOD-27359 | biostudies-arrayexpress
Project description:We prepared spinal cords from Optn floxed and KO mice treated with vehicle or the RIPK1 inhibitor Nec-1s, which were enriched for CD45+ cells and single cell RNA sequenced using the inDrop protocol.
2021-03-24 | GSE167327 | GEO
Project description:Mammalian motor circuits control voluntary movements by transmitting signals from the central nervous system (CNS) to muscle targets. To form these circuits, motor neurons (MNs) must extend their axons out of the CNS. Although motor axon exit from the CNS is an indispensable phase of motor axon pathfinding, the underlying molecular mechanisms remain obscure. Here, we present the first identification of a genetic pathway that regulates motor axon exit from the vertebrate spinal cord, utilizing spinal accessory motor neurons (SACMN) as a model system. SACMN are a homogeneous population of spinal MNs whose axons leave the CNS through a discrete lateral exit point (LEP) and can be visualized by the expression of the cell surface protein, BEN. We show that the homeodomain transcription factor, Nkx2.9, is selectively required for SACMN axon exit and identify the Robo2 guidance receptor as a likely downstream effector of Nkx2.9; loss of Nkx2.9 leads to a reduction in Robo2 mRNA and protein within SACMN and SACMN axons fail to exit the spinal cord in Robo2-deficient mice. Consistent with short-range interactions between Robo2 and Slit ligands regulating SACMN axon exit, Robo2-expressing SACMN axons normally navigate through LEP-associated Slits as they emerge from the spinal cord, and fail to exit in Slit-deficient mice. Our studies support the view that Nkx2.9 controls SACMN axon exit from the mammalian spinal cord by regulating Robo-Slit signaling. We utilized microarray technology to identify novel downstream effectors of the homeodomain transcription factor, Nkx2.9, that regulate spinal accessory motor neuron development.
2013-06-15 | E-GEOD-47953 | biostudies-arrayexpress