Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Control of osteocyte dendrite formation by Sp7 and its target gene osteocrin [RNA-Seq]

ABSTRACT: Control of osteocyte dendrite formation by Sp7 and its target gene osteocrin [RNA-Seq]

PROVIDER: PRJNA647302 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR12266800.fastq.gz	Fastqsanger.gz
	SRR12266801.fastq.gz	Fastqsanger.gz
	SRR12266802.fastq.gz	Fastqsanger.gz
	SRR12266803.fastq.gz	Fastqsanger.gz
	SRR12266804.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 18

Similar Datasets

Control of osteocyte dendrite formation by Sp7 and its target gene osteocrin [scRNA-Seq]

Project description:Some cuboidal osteoblasts differentiate into bone-embedded, dendrite-bearing osteocytes through the poorly-understood process of osteocytogenesis. Here, we report that the transcription factor Sp7 plays an essential role in osteocytogenesis. Severe defects in bone integrity and osteocyte dendrite morphology are noted in mice lacking Sp7 at the stage of the osteoblast-to-osteocyte transition. In osteocytes, Sp7 controls expression of a neuronally-enriched gene network. Analysis of the osteocyte-specific Sp7 cistrome reveals distinct genomic binding motifs and target sites distinct from those in osteoblasts. Amongst osteocyte-specific Sp7 targets, the secreted peptide osteocrin rescues Sp7-deficient defects. Single-cell transcriptional profiling of cells undergoing osteocytogenesis identifies novel Sp7-dependent transitional cell types enriched in genes linked to human fracture risk. Finally, humans with an SP7 R316C mutation display osteocyte morphology defects similar to those observed in mouse models. These findings demonstrate that cuboidal osteoblasts use a neuronally-enriched Sp7/osteocrin gene expression program to differentiate into dendrite-bearing osteocytes.

2021-09-20 | GSE154718 | GEO

Control of osteocyte dendrite formation by Sp7 and its target gene osteocrin [RNA-Seq]

2021-09-20 | GSE154717 | GEO

Control of osteocyte dendrite formation by Sp7 and its target gene osteocrin [ChIP-Seq]

2021-09-20 | GSE154716 | GEO

Control of osteocyte dendrite formation by Sp7 and its target gene osteocrin

Project description:Control of osteocyte dendrite formation by Sp7 and its target gene osteocrin

| PRJNA647296 | ENA

Control of osteocyte dendrite formation by Sp7 and its target gene osteocrin [scRNA-Seq]

Project description:Control of osteocyte dendrite formation by Sp7 and its target gene osteocrin [scRNA-Seq]

| PRJNA647304 | ENA

Control of osteocyte dendrite formation by Sp7 and its target gene osteocrin [ChIP-Seq]

Project description:Control of osteocyte dendrite formation by Sp7 and its target gene osteocrin [ChIP-Seq]

| PRJNA647303 | ENA

Control of osteocyte dendrite formation by Sp7 and its target gene osteocrin

Project description:Some osteoblasts embed within bone matrix, change shape, and become dendrite-bearing osteocytes. The circuitry that drives dendrite formation during “osteocytogenesis” is poorly understood. Here we show that deletion of Sp7 in osteoblasts and osteocytes causes defects in osteocyte dendrites. Profiling of Sp7 target genes and binding sites reveals unexpected repurposing of this transcription factor to drive dendrite formation. Osteocrin is a Sp7 target gene that promotes osteocyte dendrite formation and rescues defects in Sp7-deficient mice. Single-cell RNA-sequencing demonstrates defects in osteocyte maturation in the absence of Sp7. Sp7-dependent osteocyte gene networks are associated with human skeletal diseases. Moreover, humans with a SP7R316C mutation show defective osteocyte morphology. Sp7-dependent genes that mark osteocytes are enriched in neurons, highlighting shared features between osteocytic and neuronal connectivity. These findings reveal a role for Sp7 and its target gene Osteocrin in osteocytogenesis, revealing that pathways that control osteocyte development influence human bone diseases. The molecular circuitry that drives dendrite formation during osteocytogenesis remains poorly understood. Here the authors show that deletion of Sp7, a gene linked to rare and common skeletal disease, in mature osteoblasts and osteocytes causes severe defects in osteocyte dendrites.

| S-EPMC8560803 | biostudies-literature

Control of osteocyte dendrite formation by Sp7 and its target gene osteocrin

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

2021-09-20 | GSE154719 | GEO

Role of Piezo1-mediated mechanotransduction in osteocyte differentiation

Project description:Mechanical force is a fundamental regulator of bone development and homeostasis. Mechanosensitive osteocytes are the most abundant bone cells that form interconnected dendrites to respond to mechanical stimuli and interact with the bone-forming osteoblasts and the bone-remodeling osteoclasts. However, the molecular mechanisms underlying osteocyte maturation and dendrite formation remain unclear. By generating a Piezo1 "knock-out" osteocyte cell line, we identified a key role of Piezo1-mediated mechanotransduction in osteocyte differentiation. QRT-PCR analysis revealed delayed osteocyte differentiation in the Piezo1 KO cells relative to WT cells. By performing bulk RNA sequencing of WT and Piezo1 KO OCY454 cells at early (D1), intermediate (D14), and late (D28) stages of differentiation allowed for the identification of key signaling pathways in driving normal osteocyte dfiferentiation, as well as those regulated by Piezo1 mechanotransduction.

2024-09-20 | GSE277264 | GEO

The effect of S309W mutation on SP7 genomic binding in chondrocytes

Project description:SP7/Osterix is a transcription factor critical for osteoblast maturation and bone formation. We identidied a missense variant (c.926C>G:p.S309W) in SP7 in a patient with a unique high turnover bone disease. Mice with the corresponding variant similarly showed a complex skeletal phenotype distinct from that of Sp7-null mice. We therefore performed ChIP-Seq in primary chondrocytes to study how the mutation alters the genomic binding of SP7.

2021-12-22 | GSE151217 | GEO

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