Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Kdm6b-mediated epigenetic coordination of temporal precision during motor neuron differentiation

ABSTRACT: This SuperSeries is composed of the SubSeries listed below. GSE305831 and GSE305767.

ORGANISM(S): Mus musculus

PROVIDER: GSE306766 | GEO | 2025/09/24

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

Kdm6b-mediated epigenetic coordination of temporal precision during motor neuron differentiation [CutRun_CutTag]

Project description:Histone modifiers are crucial for instructing multiple-stage cellular differentiation, yet the mechanisms underlying their temporal precision remain enigmatic. Here, we demonstrate that the H3K27 demethylase Kdm6b acts as an epigenetic regulator, coordinating stepwise motor neuron (MN) differentiation through sequential partnerships with stage-specific transcription factors (TFs). Genome-wide profiling reveals a progressive gain in Kdm6b occupancy, especially at distal regulatory elements, as differentiation proceeds. Kdm6b dynamically shapes chromatin landscapes by coordinating H3K27me3 removal with H3K27ac and H3K4me1 acquisition, thereby enabling timed gene activation from MN specification to maturation. Stage-specific inhibition of Kdm6b compromised the ordered expression of developmental genes. Mechanistically, Kdm6b interacts with temporal TFs over time to ensure precise transcriptional control and MN differentiation. Our work elucidates how a single epigenetic regulator achieves temporal fidelity in driving stepwise MN development, and exemplifies a mechanistic insight into epigenetic regulation in determining developmental timing, with broad implications for understanding neurodevelopment and related diseases.

2025-09-24 | GSE305831 | GEO

Kdm6b-mediated epigenetic coordination of temporal precision during motor neuron differentiation [RNA-seq]

2025-09-24 | GSE305767 | GEO

Kdm6b-mediated epigenetic coordination of temporal precision during motor neuron differentiation

Project description:Kdm6b-mediated epigenetic coordination of temporal precision during motor neuron differentiation

| PRJNA1312061 | ENA

Kdm6b-mediated epigenetic coordination of temporal precision during motor neuron differentiation [CutRun_CutTag]

Project description:Kdm6b-mediated epigenetic coordination of temporal precision during motor neuron differentiation [CutRun_CutTag]

| PRJNA1307991 | ENA

Kdm6b-mediated epigenetic coordination of temporal precision during motor neuron differentiation [RNA-seq]

Project description:Kdm6b-mediated epigenetic coordination of temporal precision during motor neuron differentiation [RNA-seq]

| PRJNA1307565 | ENA

Area-specific temporal control of corticospinal motor neuron differentiation by COUP-TFI.

Project description:Transcription factors with gradients of expression in neocortical progenitors give rise to distinct motor and sensory cortical areas by controlling the area-specific differentiation of distinct neuronal subtypes. However, the molecular mechanisms underlying this area-restricted control are still unclear. Here, we show that COUP-TFI controls the timing of birth and specification of corticospinal motor neurons (CSMN) in somatosensory cortex via repression of a CSMN differentiation program. Loss of COUP-TFI function causes an area-specific premature generation of neurons with cardinal features of CSMN, which project to subcerebral structures, including the spinal cord. Concurrently, genuine CSMN differentiate imprecisely and do not project beyond the pons, together resulting in impaired skilled motor function in adult mice with cortical COUP-TFI loss-of-function. Our findings indicate that COUP-TFI exerts critical areal and temporal control over the precise differentiation of CSMN during corticogenesis, thereby enabling the area-specific functional features of motor and sensory areas to arise.

| S-EPMC2840488 | biostudies-other

Temporal control of species-specific motor neuron differentiation

Project description:This SuperSeries is composed of the SubSeries listed below.

2020-09-18 | GSE140749 | GEO

Temporal control of species-specific motor neuron differentiation [Mm]

Project description:How species-specific developmental timing is controlled is largely unknown. By following human embryonic stem cell (hESC) and mouse stem cell (mESC) differentiation to motor neurons through detailed RNA-sequencing time courses, we wish to find if there is a global scaling factor between species

2020-09-18 | GSE140748 | GEO

Temporal control of species-specific motor neuron differentiation [Hs]

2020-09-18 | GSE140747 | GEO

Allyl sulfide promotes osteoblast differentiation and bone density via reducing mitochondrial DNA release mediated Kdm6b/H3K27me3 epigenetic mechanism.

Project description:Age-associated bone loss or osteoporosis is a common clinical manifestation during aging (AG). The mechanism underlying age-associated osteoblast dysfunction induced by oxidative damage in the mitochondria and loss of bone density remains elusive. Here, we demonstrated the effect of allyl sulfide (AS), a natural organosulfur compound, on mitochondrial (mt) function in bone marrow-derived mesenchymal stem cells (BMMSCs) and bone density in AG mice. The data demonstrate that AS treatment in AG mice promotes BMMSCs differentiation and mineralization via inhibition of mitochondrial oxidative damage. The data also indicate that AG related mito-damage was associated with reduced mitochondrial biogenesis and oxidative phosphorylation, and release of a greater concentration of mtDNA. Furthermore, the data showed that mtDNA caused histone H3K27 demethylase inhibition, KDM6B, and subsequent inflammation by unbalancing mitochondrial redox homeostasis. KDM6B overexpression in AG BMMSCs or AS administration in AG mice restores osteogenesis and bone density in vitro and in vivo. Mechanistically, AS or the mitochondrial-specific antioxidant Mito-TEMPO increased KDM6B expression and upregulated the expression of Runx2 in BMMSCs, probably via epigenetic inhibition of H3K27me3 methylation at the promoter. These data uncover the previously undefined role of AS mediated prevention of mtDNA release, promoting osteogenesis and bone density via an epigenetic mechanism. Therefore, AS could be a potential drug target for the treatment of aging-associated osteoporosis.

| S-EPMC8457530 | biostudies-literature

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