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Metabolomics,Unknown,Transcriptomics,Genomics,Proteomics

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Expression data from embryonic mouse cervical spinal cords

ABSTRACT: 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.

ORGANISM(S): Mus musculus

SUBMITTER: Zaven Kaprielian

PROVIDER: E-GEOD-47953 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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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

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

Transcription profiling of rat neonatal spinal cord reveals two distinct neuronal populations

Project description:Here we compare the gene expression profiles of two distict, fluorescently identified neuronal populations, the motor neruons (MN) and the decending commissural interneurons (dCIN) of the neonatal rat spinal cord isolated with laser microdissection. These two populations participate in the neuronal networks in the spinal cord where they have destinct functions in shaping (dCINs) and transferring the output to the muscles (MNs) during locomotion. We wished to determine how the functinal differences in these nerurons are manifested at the gene expression level. Experiment Overall Design: Neurons were retrogradely labelled with rhodamine through application of the tracer to cut axons followed by incubation in oxygenated Ringer solution. Spinal cord were then snap frozen, cryosectioned and fluorescent single cells were laser dissected into a collector tube to a total of ca. 50-200 cells pr sample. RNA was then extracted, two round amplified and hybridized to Affymatrix RNU-34 chips. 22 samples were hybridized onto chips, 7 MNs, 7 CINS and 8 MIX.

2008-06-16 | E-GEOD-9439 | biostudies-arrayexpress

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

2016-06-26 | GSE75701 | GEO

Genomewide screening for pectoral fin MN specific markers

Project description:The goal of this study is to find skate pectoral fin motor neuron markers. Total RNA was extracted from manually sorted pectoral fin MNs, which were retrogradely labeled and tail spinal cord cells. By comparing RNA expression profiles of pectoral fin MNs and tail spinal cord neurons, we could identity general MN, MN columnar, and subset MN pool markers for fin MNs.

2018-02-08 | GSE105156 | GEO

Developmental and Injury-induced Changes in DNA Methylation in Regenerative versus Non-regenerative Regions of the Vertebrate (Xenopus laevis) Central Nervous System Characterized by Whole Genome Bisulfite Sequencing (WGBS)

Project description:Xenopus is uniquely suited for identifying core features of successful CNS axon regeneration, because parts of its CNS (e.g., eye), regenerate axons throughout life, whereas others (e.g., hindbrain) do so only as tadpoles. We performed bisulfite whole genome bisulfite methylation sequencing (WGBS) on juvenile frog eye after optic nerve injury, and on hindbrain samples from tadpole and juvenile frog after spinal cord injury during the peak phase of axon regeneration, to compare tissue-related and injury-induced differences in DNA methylation among them.

2022-01-05 | GSE183355 | GEO

RNAseq of fluidically isolated human and mouse motor neuron somas and axons in vitro

Project description:Spinal motor axons traverse large distances to innervate target muscle, and thus require local control of cellular events for proper functioning of the distal axon. To interrogate axon-specific processes we developed Axon-seq, a refined method incorporating microfluidic devices and stringent bioinformatic quality controls. Axon-seq demonstrates improved sensitivity and accuracy in whole-transcriptome sequencing of axons compared to previously published studies. Importantly, we show that axon transcriptomes are distinct from those of somas, displaying fewer detected genes and no contaminating astrocytic markers. We identified >5,000 transcripts in stem cell-derived spinal motor axons required for local oxidative energy production and ribosome generation. Axons contained unique transcription factor mRNAs, e.g. Ybx1, with implications for local axonal functions. Cross-comparison with existing mouse motor axon datasets, as well as our own human motor axon data identified a common axon transcriptome. As motor axons degenerate in amyotrophic lateral sclerosis (ALS), we investigated their response to the disease-causing SOD1G93A mutation, identifying 121 ALS-dysregulated transcripts. Several of these are implicated in axonal and dendritic outgrowth, including Nrp1, Dbn1, and Nek1, a known ALS-causing gene. In conclusion, Axon-seq proves a robust and improved method for RNA-seq of axons, furthers our understanding of peripheral axon biology, and identifies novel therapeutic targets to maintain neural connectivity in disease.

2018-12-11 | GSE121069 | GEO

Identify a panel of transcripts that exhibited differential expression between spinal cord motor neurons (spMNs) with low and high regenerative abilities

Project description:The mammalian neurons in the central nervous system (CNS) fail to regenerate their axons after injury, while the adult peripheral nervous system (PNS) neurons can regenerate their axons robustly. Promoting the intrinsic regenerative capacity of CNS neurons after injury is potential way to solve this difficulty. For this purpose, we have identified a panel of transcripts that exhibited differential expression between spinal cord motor neurons (spMNs) with low and high regenerative abilities by using retrograde tracing and single-cell RNA sequencing.

2022-12-30 | GSE221115 | GEO

Selective Death in Spinal Muscular Atrophy: Genome-Wide RNA-Seq Using Purified Patient-Derived Motor Neurons

Project description:Spinal Muscular Atrophy (SMA) is well-known to be caused by mutations in the gene Survival of Motor Neuron 1 (SMN1). Because this gene is ubiquitously expressed, it remains poorly understood why motor neurons (MNs) are one of the most affected cell types. To begin to address this question, we carried out RNA-sequencing studies using fixed, antibody-labeled and purified MNs produced from control and SMA patient-derived induced pluripotent stem cells (iPSCs). We found SMA-specific changes in MNs, including hyper-activation of the endoplasmic reticulum (ER) stress pathway and enhanced apoptosis. Functional studies demonstrated that inhibition of ER stress improves overall MN health and survival in vitro even in MNs with low SMN levels. In SMA mice, we show that systemic delivery of an ER stress inhibitor that crosses the blood-brain-barrier led to preservation of MNs in the spinal cord and prolonged survival of these mice. Therefore, our study implies that selective activation of ER stress underlies MN death in SMA. Moreover, the approach we have taken would be broadly applicable to studying disease-prone human cells in heterogeneous cultures. total RNA collected from ES cell and patient ES cell derived spinal motor neurons

2015-09-01 | E-GEOD-69175 | biostudies-arrayexpress

Identification of intrinsic growth modulators for intact CNS neurons after injury

Project description:Functional deficits persist after spinal cord injury (SCI) because axons in the adult mammalian central nervous system (CNS) fail to regenerate. However, modest levels of spontaneous functional recovery are typically observed after trauma, and are thought to be mediated by the plasticity of intact circuits. The mechanisms underlying intact circuit plasticity are not delineated. Here, we characterize the in vivo transcriptome of sprouting intact neurons from ngr1 null mice after partial SCI. We identify the lysophosphatidic acid signaling modulators Lppr1 and Lpar1 as intrinsic axon growth modulators for intact corticospinal motor neurons after adjacent injury. Furthermore, in vivo Lpar1 inhibition or Lppr1 overexpression enhances sprouting of intact corticospinal tract axons and yields greater functional recovery after unilateral brainstem lesion in wild type mice. Thus, the transcriptional profile of injury-induced sprouting of intact neurons reveals targets for therapeutic enhancement of axon growth initiation and new synapse formation.

2017-03-13 | GSE94482 | GEO

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