Genomewide screening for pectoral fin MN specific markers
Ontology highlight
ABSTRACT:
ORGANISM(S): Leucoraja erinaceus
PROVIDER: GSE105156 | GEO | 2018/02/08
REPOSITORIES: GEO
Similar Datasets
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
Project description:Genomewide screening for pectoral fin MN specific markers
| PRJNA414974 | ENA
Project description:Spinal cord injury leads to impaired motor and sensory functions. After spinal cord injury there is a an initial phase of hypo-reflexia followed by a developing hyper-reflexia, often termed spasticity. Previous studies have suggested a relationship between the reappearance of plateau potentials in motor neurons and the development of spasticity after spinalization. To understand the molecular mechanism behind this phenomena we examined the transcriptional response of the motor neurons after spinal cord injury as it progress over time. We used a rat tail injury model where a complete transection of the caudal (S2) rat spinal cord leads to an immediate flaccid paralysis of the tail and a subsequent appearance of spasticity 2-3 weeks post injury that develops into strong spasticity after 2 months. Gene expression changes were studied in motor neurones 0, 2, 7, 21 and 60 days after complete spinal transection. Tail MNs were retrogradely labelled with Fluoro-Gold injected into the muscle and intra peritoneally. 5-7 days after tracer injections the spinal cord was dissected out, snap-frozen in liquid nitrogen, sliced in 10 um thick slices and fluorescent motor neurons 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 Affymetrix rat 230 2.0 arays. 31 samples were hybridized onto chips, 4 Spi-0 (Control), 6 Spi-2, 5 Spi-7, 8 Spi-21 and 8 Spi-60.
2010-05-27 | E-GEOD-19701 | biostudies-arrayexpress
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
Project description:Combinatorial transcription codes generate the myriad of cell types during development, and thus likely provide crucial insights into directed differentiation of stem cells to a specific cell type. The LIM-complex composed of Isl1 and Lhx3 directs the specification of spinal motor neurons (MNs) in embryos. Here, we report that Isl1-Lhx3, a LIMcomplex-mimicking fusion, induces a signature of MN transcriptome and concomitantly suppresses interneuron differentiation programs, thereby serving as a potent and specific inducer of MNs in stem cells. We show that an equimolar ratio of Isl1 and Lhx3 and the LIM-domain of Lhx3 are crucial for generating MNs without upregulating interneuron genes. These led us to design Isl1-Lhx3, which maintains the desirable 1:1 ratio of Isl1 and Lhx3 and the LIM-domain of Lhx3. Isl1-Lhx3 drives MN differentiation with high specificity and efficiency in the spinal cord and embryonic stem cells, bypassing the need for sonic hedgehog. RNA-seq analysis revealed that Isl1-Lhx3 induces the expression of a battery of MN genes that control various functional aspects of MNs, while suppressing key interneuron genes. Our studies uncover a highly efficient method for directed MN generation and MN gene networks. Our results also demonstrate a general strategy of utilizing embryonic transcription complexes for producing specific cell types from stem cells. Examine the RNA expression profiles of inducible motor neurons-embryonic stem cells (iMN-ESCs) with or without Dox treatment, with biological duplicates.
2012-02-03 | E-GEOD-35510 | biostudies-arrayexpress
Project description:To identify gender specific differences in gene expression during fin rgeneration, pectoral fins were amputated from both male and female adult fish. Fins were allowed to recover for 4 days in standard tank condtions then tissue was collected for RNA isolation and microarray analysis Pooled samples from male and females, injured and uninjured in biological trilicate.
2011-09-02 | E-GEOD-31871 | biostudies-arrayexpress
Project description:To identify gender specific differences in gene expression during fin rgeneration, pectoral fins were amputated from both male and female adult fish. Fins were allowed to recover for 4 days in standard tank condtions then tissue was collected for RNA isolation and microarray analysis
2011-09-03 | GSE31871 | GEO
Project description:Amyotrophic lateral sclerosis (ALS) is an incurable neurological disease featuring progressive loss of motor neuron (MN) function in the brain and spinal cord. Mutations in TARDBP, encoding the RNA-binding protein TDP-43, are one cause of ALS and TDP-43 mislocalization in MNs is a key pathological feature of >95% of ALS cases. While numerous studies support altered RNA regulation by TDP-43 as a major cause of disease, specific changes within MNs that trigger disease onset remain unclear. Here, we combined Translating Ribosome Affinity Purification (TRAP) with RNA sequencing to identify molecular changes in spinal MNs of TDP-43–driven ALS at motor symptom onset. By comparing the MN translatome of hTDP-43A315T mice to littermate controls and to mice expressing wildtype hTDP-43, we identify hundreds of mRNAs that were selectively up- or downregulated in MNs. We validated effects on Tex26, Syngr4, and Plekhb1 mRNAs in an independent TRAP experiment. Moreover, by quantitative immunostaining of spinal cord MNs we found corresponding protein level changes for SYNGR4 and PLEKHB1. We also observed these changes in spinal MNs of an independent ALS mouse model caused by a different patient mutant allele of TDP-43, suggesting that they may be a general feature of TDP-43-driven ALS. Thus, we have identified two new proteins deregulated in MNs at motor symptom onset in TDP-43-driven ALS models. This spatial and temporal pattern suggests that deregulation of these proteins could be functionally important for driving the transition to the symptomatic phase of disease.
2023-01-01 | GSE144640 | GEO
Project description:Single cell dataset of human motor neurons laser-captured from postmortem ALS and control tissues
(1) ALS Pilot dataset
(2) TDP43 stratified dataset
Summary: Unbiased proteomics has been employed to interrogate central nervous system (CNS) tissues (brain, spinal cord) and fluid matrices (CSF, plasma) from amyotrophic lateral sclerosis (ALS) patients; yet, a limitation of conventional bulk tissue studies is that motor neuron (MN) proteome signals may be confounded by admixed non-MN proteins. Recent advances in trace sample proteomics have enabled quantitative protein abundance datasets from single human MNs (Cong et al., 2020b). In this study, we leveraged laser capture microdissection (LCM) and nanoPOTS (Zhu et al., 2018c) single-cell mass spectrometry (MS)-based proteomics to query changes in protein expression in single MNs from postmortem ALS and control donor spinal cord tissues, leading to the identification of 2515 proteins across MNs samples (>900 per single MN) and quantitative comparison of 1870 proteins between disease groups. Furthermore, we studied the impact of enriching/stratifying MN proteome samples based on the presence and extent of immunoreactive, cytoplasmic TDP-43 inclusions, allowing identification of 3368 proteins across MNs samples and profiling of 2238 proteins across TDP-43 strata. We found extensive overlap in differential protein abundance profiles between MNs with or without obvious TDP-43 cytoplasmic inclusions that together point to early and sustained dysregulation of oxidative phosphorylation, mRNA splicing and translation, and retromer-mediated vesicular transport in ALS. Our data are the first unbiased quantification of single MN protein abundance changes associated with TDP-43 proteinopathy and begin to demonstrate the utility of pathology-stratified trace sample proteomics for understanding single-cell protein abundance changes in human neurologic diseases.
2023-06-07 | MSV000092119 | MassIVE
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