Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Expression data from control or Hnf6/Oc2 compound mutant mouse embryonic spinal cords

ABSTRACT: 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

ORGANISM(S): Mus musculus

PROVIDER: GSE117871 | GEO | 2018/07/31

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Similar Datasets

Expression data from control or conditional Oc-deficient embryonic motor neurons

Project description:In the embryonic spinal cord, motor neurons diversify into different subsets characterized by distinct molecular identity, localization and connectivity. However, the factors that control MN diversification remain poorly known. To identify genes downstream of Onecut transcription factors in motor neurons that may contribute to motor neuron diversification, we performed a RNA-sequencing comparison of control and of OC-deficient motor neuron transcriptome at embryonic day 10.5.

2019-12-13 | GSE141949 | GEO

Expression data from embryonic mouse cervical spinal cords

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

Expression data from embryonic mouse spinal cords from NFIX knockout and wild-type mice.

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

Genome wide analysis of upper spinal cords with training after spinal cord hemisection injury

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

Expression data from embryonic mouse cervical spinal cords

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.

2013-06-15 | GSE47953 | GEO

Gene expression in experimentally injured and control mouse spinal cords

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

Human expression data from iPSCs, motor neurons derived from iPSCs and ESCs, and fetal spinal cords

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

Expression data from ICR mouse spinal cords - normal or injured spinal cord

Project description:LncRNAs played a crucial role in the cell growth, development and some diseases relating to central nerve system.This study suggest that with regulating the LncRNAs expression level we might design novel therapy for spinalcord injury. In this dataset, we profiled the expression pattern of LncRNAs by microarray method after spinal cord injury (SCI). Through Gene ontology and Kyoto Encyclopedia of Genes and Genomes enrichment analysis seek LncRNAs potential function in the repair of spinal cord injury.

2015-09-01 | GSE67515 | GEO

Human expression data from iPSCs, motor neurons derived from iPSCs and ESCs, and fetal spinal cords

2016-06-26 | GSE75701 | GEO

A CpG mutational hotspot in a ONECUT (HNF6) binding site accounts for the prevalent variant of Hemophilia B Leyden

Project description:Hemophilia B, or the 'Royal Disease', arises from mutations in the Coagulation Factor IX (F9) gene. Mutations within the F9 promoter are associated with a remarkable form of the disease, termed Hemophilia B Leyden, in which symptoms ameliorate after puberty. Mutations at the -5/-6 site account for the majority of Leyden cases, and have been postulated to disrupt the binding of a transcriptional activator, the identity of which has remained elusive for more than twenty years. Here we show that the ONECUT transcription factors (ONECUT1/HNF6 and ONECUT2/HNF6B) bind to the -5/-6 site. The various Hemophilia B Leyden mutations that have been reported in this site inhibit ONECUT binding to varying degrees that correlate well with their associated clinical severities. In addition, expression of F9 is crucially dependent on ONECUT factors in vivo and as such, mice that are deficient in either ONECUT1, ONECUT2 or both, exhibit depleted levels of F9. Taken together, our findings establish the ONECUT transcription factors as the missing regulators of Hemophilia B Leyden that operate through the -5/-6 site.

2013-03-06 | E-MTAB-890 | biostudies-arrayexpress

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data