Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

14 days old 2310061I04Rik-null brain transcriptome

ABSTRACT: Here, we describe a spontaneous mouse mutant with a deletion in a predicted gene 2310061I04Rik (Rik) of unknown function located on chromosome 17. A 59 base pair long deletion occurred in the first intron of the Rik gene and disrupted its expression. Riknull mice were born healthy and appeared anatomically normal up to two weeks of age. After that, these mice showed inhibited growth, ataxic gait, and died shortly after postnatal day 24 (P24). Transcriptome analysis at P14 and P23 revealed significantly reduced expression of mitochondrial genes in Riknull brains compared to wild type controls including mt-Nd4, mt-Cytb, mt-Nd2, mt-Co1, mt-Atp6, and others. Similarly, genes specific for myelinating oligodendrocytes also showed reduced expression in P23 Riknull brains compared to controls. Histological examination of anterior thalamic nuclei demonstrated decreased myelination of anteroventral nuclei but not of anterodorsal nuclei in P23 Riknull mice. Myelination of the anterior commissure was also impaired and displayed extensive vacuolation. Consistently with these findings, immunohistochemistry showed reduced expression of Opalin, a glycoprotein expressed in differentiated oligodendrocytes. Taken together, these results suggest that RIK is important for oligodendrocyte maturation and myelination in the developing brain.

ORGANISM(S): Mus musculus

PROVIDER: GSE275372 | GEO | 2024/12/05

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

E9.5 TRAF7-*/-* brain transcriptome

Project description:Here, we describe a spontaneous mouse mutant with a deletion in a predicted gene 2310061I04Rik (Rik) of unknown function located on chromosome 17. A 59 base pair long deletion occurred in the first intron of the Rik gene and disrupted its expression. Riknull mice were born healthy and appeared anatomically normal up to two weeks of age. After that, these mice showed inhibited growth, ataxic gait, and died shortly after postnatal day 24 (P24). Transcriptome analysis at P14 and P23 revealed significantly reduced expression of mitochondrial genes in Riknull brains compared to wild type controls including mt-Nd4, mt-Cytb, mt-Nd2, mt-Co1, mt-Atp6, and others. Similarly, genes specific for myelinating oligodendrocytes also showed reduced expression in P23 Riknull brains compared to controls. Histological examination of anterior thalamic nuclei demonstrated decreased myelination of anteroventral nuclei but not of anterodorsal nuclei in P23 Riknull mice. Myelination of the anterior commissure was also impaired and displayed extensive vacuolation. Consistently with these findings, immunohistochemistry showed reduced expression of Opalin, a glycoprotein expressed in differentiated oligodendrocytes. Taken together, these results suggest that RIK is important for oligodendrocyte maturation and myelination in the developing brain.

2024-12-05 | GSE275376 | GEO

23 days old 2310061I04Rik-null brain transcriptome

2024-12-05 | GSE275375 | GEO

SRF transcriptionally regulates the oligodendrocyte cytoskeleton during CNS myelination (snRNA-Seq)

Project description:Myelination of neuronal axons is essential for nervous system development. Myelination requires dramatic cytoskeletal dynamics in oligodendrocytes, but how actin is regulated during myelination is poorly understood. We recently identified serum response factor (SRF)—a transcription factor known to regulate expression of actin and actin regulators in other cell types—as a critical driver of myelination in the aged brain. Yet, a major gap remains in understanding the fundamental role of SRF in oligodendrocyte lineage cells. Here we show that SRF is required cell autonomously in oligodendrocytes for myelination during development. Combining ChIP-seq with RNA-seq identifies SRF-target genes in OPCs and oligodendrocytes that include actin and other key cytoskeletal genes. Accordingly, SRF knockout oligodendrocytes exhibit dramatically reduced actin filament levels early in differentiation, consistent with its role in actin-dependent myelin sheath initiation. Together, our findings identify SRF as a transcriptional regulator that controls the expression of cytoskeletal genes required in oligodendrocytes for myelination. This study identifies a novel pathway regulating oligodendrocyte biology with high relevance to brain development, aging, and disease.

2024-02-23 | GSE243678 | GEO

SRF transcriptionally regulates the oligodendrocyte cytoskeleton during CNS myelination (RNA-Seq)

2024-02-23 | GSE241560 | GEO

SRF transcriptionally regulates the oligodendrocyte cytoskeleton during CNS myelination (ChIP-Seq)

2024-02-23 | GSE241559 | GEO

Single nuclei transcriptomic profiling of human astrocytes and oligodendrocytes in Alzheimer’s disease I

Project description:Single nuclei RNA sequencing (snRNA-seq) dataset characterizing astrocytes and oligodendrocytes isolated from human postmortem APOE e2/3 Alzheimer's disease (AD) and aged-matched non-symptomatic (NS) brains.

2022-04-01 | GSE167490 | GEO

Genome-wide mapping of Olig2 targets in primary oligodendrocytes

Project description:Myelination by oligodendrocytes in the central nervous system (CNS) is essential for proper brain function, yet the molecular determinants that control this process remain poorly understood. The basic helix-loop-helix transcription factors Olig1 and Olig2 promote myelination, whereas bone morphogenetic protein (BMP) and Wnt/?-catenin signaling inhibit myelination. Here we show that these opposing regulators of myelination are functionally linked by the Olig1/2 common target Smad-interacting protein-1 (Sip1). We demonstrate that Sip1 is an essential modulator of CNS myelination. Sip1 represses differentiation inhibitory signals by antagonizing BMP receptor-activated Smad activity while activating crucial oligodendrocyte-promoting factors. Importantly, a key Sip1-activated target, Smad7, is required for oligodendrocyte differentiation and partially rescues differentiation defects caused by Sip1 loss. Smad7 promotes myelination by blocking the BMP- and ?-catenin-negative regulatory pathways. Thus, our findings reveal that Sip1-mediated antagonism of inhibitory signaling is critical for promoting CNS myelination and point to new mediators for myelin repair. ChIP-seq was performed to identify Olig2 direct target genes in oligodendrocytes during oligodendrocyte differentiation.

2012-08-31 | E-GEOD-40506 | biostudies-arrayexpress

Single-nucleus transcriptome analysis reveals dysregulation of angiogenic endothelial cells and neuroprotective glia in Alzheimer's disease

Project description:Alzheimer’s disease (AD) is the most common form of dementia but has no effective treatment. A comprehensive investigation of cell-type-specific responses and cellular heterogeneity in AD is required to provide precise molecular and cellular targets for therapeutic development. Accordingly, we perform single-nucleus transcriptome analysis of 169,496 nuclei from the prefrontal cortical samples of AD patients and normal control (NC) subjects. Differential analysis shows that the cell-type-specific transcriptomic changes in AD are associated with the disruption of biological processes including angiogenesis, immune activation, synaptic signaling, and myelination. Subcluster analysis reveals that compared to NC brains, AD brains contain fewer neuroprotective astrocytes and oligodendrocytes. Importantly, our findings show that a subpopulation of angiogenic endothelial cells is induced in the brain in patients with AD. These angiogenic endothelial cells exhibit increased expression of angiogenic growth factors and their receptors (i.e., EGFL7, FLT1, and VWF) and antigen-presentation machinery (i.e., B2M and HLA-E). This suggests that these endothelial cells contribute to angiogenesis and immune response in AD pathogenesis. Thus, our comprehensive molecular profiling of brain samples from patients with AD reveals previously unknown molecular changes as well as cellular targets that potentially underlie the functional dysregulation of endothelial cells, astrocytes, and oligodendrocytes in AD, providing important insights for therapeutic development.

2020-09-28 | GSE157827 | GEO

Opposite roles for astrocytes in developmental myelination and early myelin repair

Project description:Understanding the regulation of oligodendrocyte development and myelination in the central nervous system (CNS) is essential, not only to facilitate myelin repair but also to define the role of oligodendrocytes in maintaining axonal integrity. In vitro studies have implicated astrocytes in influencing multiple aspects of oligodendrocytes and their precursors, however the in vivo role of astrocytes in myelination and myelin repair remain poorly defined. We show that astrocyte ablation during postnatal spinal cord development resulted in a concomitant delay in myelination, demonstrating a critical role for astrocytes in promoting developmental myelination. By contrast, in the adult CNS, localized ablation of astrocytes 2 days after a demyelinating insult resulted in increased numbers of oligodendrocytes and accelerated remyelination in both the spinal cord and the corpus callosum. Microarray analysis reveals astrocytic NF-kB signaling pathway as a major contributor to pathological events occurring after demyelination. We suggest that the localized functions of astrocytes are fundamentally different during developmental myelination and myelin repair. Astrocytes are critical for developmental myelination, however in a demyelinating environment they are detrimental to myelin repair.

2017-08-01 | GSE60276 | GEO

Genome-wide maps of Wnt effector Tcf7l2/Tcf4 occupancy in oligodendrocyte during CNS myelination

Project description:We performed genome-wide profiling of Tcf7l2 occupancy during oligodendrocyte differentiation and identified the key enzymes involved in cholesterol metabolism and essential for CNS myelination. Examination of Tcf7l2 chIP-seq in oligodendrocyte progenitor cell and 2 differentiation oligodendrocytes.

2016-02-19 | E-GEOD-65119 | biostudies-arrayexpress

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

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