Sex-Specific Astrocyte Regulation of Spinal Motor Circuits by Nkx6.1 [H3K27ac ChIP-seq]
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA1189800 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Sex-Specific Astrocyte Regulation of Spinal Motor Circuits by Nkx6.1 [Nkx6.1 ChIP-seq]
| PRJNA1189801 | ENA
Project description:To profile gene expression expresion in astrocytes between control and Nkx6.1 conditional knockout astrocytes in the mouse spinal cord. Furthermore, we sought to profile DNA binding patterns regulated by Nkx6.1 in spinal cord astrocyte.
2024-12-05 | GSE282687 | GEO
Project description:Sex-Specific Astrocyte Regulation of Spinal Motor Circuits by Nkx6.1 [RNA-seq]
| PRJNA1189799 | ENA
Project description:To examined the epigenetic alteration in male Nkx6.1 control and cKO spinal cord astrocytes
2024-12-05 | GSE282688 | GEO
Project description:To profile gene expression expresion in astrocytes between control and Nkx6.1 conditional knockout astrocytes in the mouse spinal cord.
2024-12-05 | GSE282689 | GEO
Project description:Production of learned vocalizations requires precise selection and accurate sequencing of appropriate vocal-motor actions. The basal ganglia are essential for the selection and sequencing of motor actions, but the cellular specializations and circuit mechanisms governing accurate sequencing of vocalizations are unknown. Here, we use single-nucleus RNA sequencing and genetic manipulations to map basal ganglia cell types and circuits involved in the production of songbird vocal sequences. We identify cell-type specializations in direct-like and indirect-like basal ganglia pathways, including evolutionary expansion of striatal and arkypallidal cell-types that could facilitate vocal sequencing. We also reversibly reduced the expression of FoxP2 with a viral knockdown. For birds in which FoxP2 was knocked down, striatal neurons exhibited decreased expression of Drd1 and showed an increased ratio of Drd2/Drd1 expression. These findings identify key evolutionary specializations and circuits essential for selection and sequencing of vocal-motor actions necessary for vocal communication.
2021-05-19 | GSE136086 | GEO
Project description:Nkx2.2, Nkx6.1, and Olig2 are transcriptional repressors regulating somatic motor neuron and interneuron subtypes in neural progenitors. The purpose of this study was to identify their target genes and to elucidate their gene regulatory mechanisms, including their relationship to Sonic Hedgehog/Gli pathway.
2015-08-24 | GSE61673 | GEO
Project description:Astrocytes, the most abundant cells in the central nervous system, promote synapse formation and help refine neural connectivity. Although they are allocated to spatially distinct regional domains during development, it is unknown whether region-restricted astrocytes are functionally heterogeneous. Here we show that postnatal spinal cord astrocytes express several region-specific genes, and that ventral astrocyte-encoded Semaphorin3a (Sema3a) is required for proper motor neuron and sensory neuron circuit organization. Loss of astrocyte-encoded Sema3a led to dysregulated α−motor neuron axon initial segment orientation, markedly abnormal synaptic inputs, and selective death of α−but not of adjacent γ−motor neurons. Additionally, a subset of TrkA+ sensory afferents projected to ectopic ventral positions. These findings demonstrate that stable maintenance of a positional cue by developing astrocytes influences multiple aspects of sensorimotor circuit formation. More generally, they suggest that regional astrocyte heterogeneity may help to coordinate postnatal neural circuit refinement. 12 total samples consisting of three biological replicates each of flow sorted postnatal day 7 dorsal spinal cord astrocytes, ventral spinal cord astrocytes, dorsal SC non astrocytes, and ventral SC non astrocytes
2014-05-02 | E-GEOD-55054 | biostudies-arrayexpress
Project description:This datased was used to obtain a genome-wide expression signature for the early response of mouse motor neurons to mutant SOD1 astrocytes conditioned media. Neurons, far from living in isolation, are surrounded by a host of other neuronal and non-neuronal cells, such as astrocytes. The latter entertain complex functional interactions with neighboring neurons, which, under normal conditions, are important for the their well-being. In pathological situations, however, altered astrocyte behavior may contribute to the demise of neighboring neurons. Such non-cell autonomous pathogenic scenario is increasingly considered in a variety of disorders, including amyotrophic lateral sclerosis (ALS), the most frequent adult-onset paralytic disorder. Assembly and interrogation of gene regulatory models has helped elucidate causal mechanisms responsible for the presentation of several tumor-related phenotypes. To systematically elucidate the effectors of neurodegeneration in a model of ALS, we first developed techniques for the efficient purification of motor neurons (MNs), the primary target of ALS neurodegenerative process. We then generated gene expression profiles to fully characterize the critical timepoints associated with initiation and commitment of MN degenerative progression in an in vitro murine mutant SOD1 (mSOD1) model of ALS. ES cells were derived from transgenic Hlxb9-GFP1Tmj mice expressing eGFP and CD2 driven by the mouse HB9 promoter. These cells were then differentiated into motor neurons (ES-MN) as described previously [PMID 12176325] ES-MN were exposed to non-transgenic (NTg), G93A mutant SOD1 (mSOD1) or wtSOD1 over-expression astrocytes conditioned media for 0 days (time zero control), 1 day, and 3 days. Total RNA was extracted and profiled by RNAseq.
2014-12-17 | E-GEOD-49023 | biostudies-arrayexpress
Project description:Diverse subpopulations of astrocytes tile different brain regions to accommodate local requirements of neurons and associated neuronal circuits. Nevertheless, molecular mechanisms governing astrocyte diversity remain mostly unknown. We explored the role of a zinc finger transcription factor Yin Yang 1 (YY1) that is expressed in astrocytes. We found that specific deletion of YY1 from astrocytes causes severe motor deficits in mice, induces Bergmann gliosis, and results in simultaneous loss of GFAP expression in velate and fibrous cerebellar astrocytes. Single cell RNA-seq analysis showed that YY1 exerts specific effects on gene expression in subpopulations of cerebellar astrocytes. We found that although YY1 is dispensable for the initial stages of astrocyte development, it regulates subtype-specific gene expression during astrocyte maturation. Moreover, YY1 is continuously needed to maintain astrocyte identity in the adult cerebellum. Our findings suggest that YY1 plays critical roles regulating cerebellar astrocyte maturation during development and maintaining a mature phenotype of astrocytes in the adult cerebellum.
2022-04-01 | GSE166792 | GEO