MicroRNA mechanisms instructing Purkinje cell specification
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA1224277 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR26073975.fastq.gz | Fastqsanger.gz | |||
| SRR26073977.fastq.gz | Fastqsanger.gz | |||
| SRR26073978.fastq.gz | Fastqsanger.gz | |||
| SRR26073979.fastq.gz | Fastqsanger.gz | |||
| SRR26073980.fastq.gz | Fastqsanger.gz |
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Project description:This SuperSeries is composed of the SubSeries listed below.
2025-04-02 | GSE289736 | GEO
Project description:Molecular Mechanisms of Purkinje Cell Degeneration in Ataxia-Telangiectasia
| PRJNA762121 | ENA
Project description:We performed gene-expression analysis of mouse Purkinje cells as a model M-bM-^@M-^\single-type neuronM-bM-^@M-^]. DNA microarray analysis detected at least 7,055 genes in Purkinje cells, most of which are classified into functional molecule categories. Our comparative analysis between Purkinje cells and the granule cell layer showed that the characteristic expression pattern in Purkinje cells was particularly represented by M-bM-^@M-^\the neural communication systemM-bM-^@M-^] components. Pukinje cells and granule cell layer of the mouse cerebellum were collected by laser microdissection for RNA extraction and hybridization on Affymetrix microarrays.
2013-01-17 | E-GEOD-26749 | biostudies-arrayexpress
Project description:Affymetrix array gene expression analysis using RNA isolated from Purkinje cells and ventricular myocytes from the Cntn2-EGFP/ a-MHC-Cre/ floxed-tdTomato compound transgenic dual fluorescence reporter mouse Cardiac Purkinje cells are important triggers of ventricular arrhythmias associated with heritable and acquired syndromes. The mechanisms responsible for this pro-arrhythmic behavior are incompletely understood. Here, through transcriptional profiling of genetically labeled cardiomyocytes, we identified expression of Purkinje cell protein-4 (Pcp4), a putative regulator of calmodulin and Ca2+/calmodulin-dependent kinase II (CaMKII) signaling, exclusively within the His-Purkinje network. Using Pcp4-null mice and acquired cardiomyopathy models, we demonstrate that reduced expression of PCP4 is associated with CaMKII activation, abnormal electrophysiology, dysregulated intracellular calcium handling and pro-arrhythmic behavior in isolated Purkinje cells. We also show that Pcp4-null mice display profound autonomic dysregulation and arrhythmic behavior in vivo. Together, these results demonstrate that PCP4 regulates cardiac excitability through both Purkinje cell autonomous and central mechanisms and identify this modulator of CaMKII signaling as a potential arrhythmia-susceptibility candidate.
2014-11-30 | GSE60987 | GEO
Project description:The signalling protein PKCγ is a major regulator of Purkinje cell development and synaptic function. We have shown previously that increased PKCγ activity impairs dendritic development of cerebellar Purkinje cells. Mutations in the protein kinase Cγ gene (PRKCG) cause spinocerebellar ataxia type 14 (SCA14). In a transgenic mouse model of SCA14 expressing the human S361G mutation, Purkinje cell dendritic development is impaired in cerebellar slice cultures similar to pharmacological activation of PKC. The mechanisms of PKCγ-driven inhibition of dendritic growth are still unclear. Using immunoprecipitation-coupled mass spectrometry analysis we have identified Collapsin Response Mediator Protein 2 (CRMP2) as a protein interacting with constitutive active PKCγ(S361G) and confirmed the interaction with the Duolink™ proximity ligation assay. We show that in cerebellar slice cultures from PKCγ(S361G)- mice, phosphorylation of CRMP2 at the known PKC target site Thr555 is increased in Purkinje cells confirming phosphorylation of CRMP2 by PKCγ. miRNA-mediated CRMP2 knockdown decreased Purkinje cell dendritic outgrowth in dissociated cerebellar cultures as did the transfection of CRMP2 mutants with a modified Thr555 site. In contrast, dendritic development was normal after wildtype CRMP2 overexpression. In a novel knock-in mouse expressing only the phospho-defective T555A-mutant CRMP2, Purkinje cell dendritic development was reduced in dissociated cultures. This reduction could be rescued by transfecting wildtype CRMP2 but only partially by the phospho-mimetic T555D-mutant. Our findings establish CRMP2 as an important target of PKCγ phosphorylation in Purkinje cells mediating its control of dendritic development. Dynamic regulation of CRMP2 phosphorylation via PKCγ is required for its correct function.
2022-02-24 | PXD020124 | Pride
Project description:The transcriptional events driving specification of the kidney have been well characterized. However, it remains undetermined how initial kidney field size is established, patterned, and proportioned. Lhx1 is a transcription factor expressed in the kidney anlage and is required for specification of the kidney field, but few Lhx1 interacting cofactors or downstream targets have been identified. By tandem-affinity purification, we isolated Furry (FRY), a multifunctional protein that acts as a transcriptional co-repressor of microRNAs. We found that Xenopus embryos depleted of fry exhibit loss of the kidney field, phenocopying the lhx1 depleted animals. In addition, we demonstrated synergism between Fry and Lhx1, identified candidate microRNAs regulated by the pair, and confirmed these microRNA clusters influence specification of the kidney field. Therefore, our data shows that a tissue-specific transcription factor, Lhx1, interacts with a broadly expressed microRNA repressor, Fry, to establish the kidney field.
2019-11-11 | PXD006926 | Pride
Project description:We performed gene-expression analysis of mouse Purkinje cells as a model “single-type neuron”. DNA microarray analysis detected at least 7,055 genes in Purkinje cells, most of which are classified into functional molecule categories. Our comparative analysis between Purkinje cells and the granule cell layer showed that the characteristic expression pattern in Purkinje cells was particularly represented by “the neural communication system” components.
2013-01-17 | GSE26749 | GEO
Project description:The assembly of neural circuits involves multiple sequential steps such as the specification of cell types, their migration to proper brain locations, morphological and physiological differentiation, and the formation and maturation of synaptic connections. This intricate and often prolonged process is guided by elaborate genetic mechanisms that regulate each developmental event. Evidence from numerous systems suggests that each cell type, once specified, is endowed with a genetic program that directs its subsequent development. This cell intrinsic program unfolds in respond to, and is regulated by, extrinsic signals, including cell-cell and synaptic interactions. To a large extent, the execution of this genetic program is achieved by the expression of specific sets of genes that support distinct developmental processes. Therefore, a comprehensive analysis of the developmental progression of gene expression in synaptic partners of neurons may provide a basis for exploring the genetic mechanisms regulating circuit assembly. Here we examined the developmental gene expression profiles in well defined cell types in a stereotyped microcircuit of the cerebellar cortex. Manually sorted pure populations of Purkinje cells and Stellate/Basket cells, 3 biological replicates, from Gad67-GFP bac-transgenic (G42) mice were profiled during postnatal developmental stages P3, P7, P14, P21, P28, P35 and P56 using Affymetrix MOE430.2 expression array
2012-07-19 | E-GEOD-37055 | biostudies-arrayexpress
Project description:Understanding the mechanisms of myogenesis in human induced pluripotent stem cells (hiPSCs) is a prerequisite to achieving patient-specific therapy for diseases of skeletal muscle. hiPSCs of different origin show distinctive kinetics and ability to differentiate into myocytes. To address the unique cellular and temporal context of hiPSC differentiation, we perform a longitudinal comparison of the transcriptomic profiles of three hiPSC lines that display differential myogenic specification, one robust and two blunted. We detail temporal differences in mechanisms that lead to robust myogenic specification. We show gene expression signatures of putative cell subpopulations and extracellular matrix components that may support myogenesis. Further, we show that targeted knockdown of ZIC3 at the outset of differentiation leads to improved myogenic specification in blunted hiPSC lines. Our study suggests that β-catenin transcriptional cofactors mediate crosstalk between multiple cellular processes and exogenous cues to facilitate specification of hiPSCs to mesoderm lineage, leading to robust myogenesis.
2021-03-01 | GSE161025 | GEO
Project description:Temporal mechanisms of myogenic specification in human induced pluripotent stem cells
| PRJNA675129 | ENA