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Ribosome biogenesis controls suture mesenchymal stem cell fate via selective regulation of complement pathway in to prevent craniosynostosis [RNA-seq]

ABSTRACT: Ribosome biogenesis controls suture mesenchymal stem cell fate via selective regulation of complement pathway in to prevent craniosynostosis [RNA-seq]

PROVIDER: PRJNA926977 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR23204135_1.fastq.gz	Fastqsanger.gz
	SRR23204135_2.fastq.gz	Fastqsanger.gz
	SRR23204136_1.fastq.gz	Fastqsanger.gz
	SRR23204136_2.fastq.gz	Fastqsanger.gz
	SRR23204137_1.fastq.gz	Fastqsanger.gz

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Ribosome biogenesis controls suture mesenchymal stem cell fate via selective regulation of complement pathway in to prevent craniosynostosis [RNA-seq]

Project description:Suture mesenchymal stem cell (MSC) drives calvarial suture development, homeostasis, and regeneration. Its loss leads to craniosynostosis, a prevailing craniofacial disorder characterized by premature suture closure. Ribosome biogenesis, historically thought to be a static house-keeping process, is now known to have tissue-specific roles. However, the functional specificity of ribosome biogenesis in suture MSCs remains largely unexplored, hampering development of therapeutic strategies for craniofacial tissue regeneration. We genetically perturb ribosome biogenesis using Snord118, a small nucleolar RNA (snoRNA) required for ribosomal RNA (rRNA) maturation. MSC specific conditional knockout (cKO) of Snord118 in mice leads to p53 activation, cell death, mesenchymal and MSC loss, impaired osteogenic and osteoclastic activity, resulting in suture growth and craniosynostosis defects. Using our newly established human induced pluripotent stem cell (iPSC)-derived MSCs combined with ribosome profiling, we found that SNORD118deficiency in MSCs causes global translation dysregulations and downregulation of complement pathway, a part of innate immune system with selective but poorly characterized physiological functions in craniofacial tissue homeostasis. Overall, ribosome biogenesis controls suture MSC fate via selective regulation of complement pathway.

2023-12-20 | GSE223614 | GEO

Ribosome biogenesis controls suture mesenchymal stem cell fate via selective regulation ofcomplement pathway in to prevent craniosynostosis [Ribo-seq]

2023-12-20 | GSE223615 | GEO

Ribosome biogenesis controls suture mesenchymal stem cell fate via selective regulation of complement pathway in to prevent craniosynostosis

Project description:Ribosome biogenesis controls suture mesenchymal stem cell fate via selective regulation of complement pathway in to prevent craniosynostosis

| PRJNA926976 | ENA

Ribosome biogenesis controls suture mesenchymal stem cell fate via selective regulation ofcomplement pathway in to prevent craniosynostosis [Ribo-seq]

Project description:Ribosome biogenesis controls suture mesenchymal stem cell fate via selective regulation ofcomplement pathway in to prevent craniosynostosis [Ribo-seq]

| PRJNA926978 | ENA

Skeletal Stem Cell Powering Cranial Suture Fate: An Answer to Craniosynostosis (scRNA-seq)

Project description:Purpose: The cranial suture is a fibrous joint, and similar to the growth plates of the skeletal long bone, they serve as the major centers of calvarial vault morphogenesis. Our group’s identification of a skeletal stem cell isolated from the mouse tibial growth plate prompted us to investigate whether these skeletal stem cells are also resident in the mouse cranial sutures and if they govern postnatal suture patency or fusion. Results: We preformed a spatio-temporal profiling of the mouse cranial sutures by flow cytometry, demonstrating a significant decrease in the temporal representation of skeletal stem cells in fusing versus patent sutures. Moreover, canonical Wnt signaling has a significant impact on skeletal stem cells proliferation and thus representation within the suture, dictating fate: fusion or patency. Breeding an Axin2+/-LacZ mouse, with enhanced activation of canonical Wnt signaling to a Twist1+/− mouse, harboring a coronal craniosynostosis enriched the skeletal stem cell pool in coronal sutures, thereby preventing Twist1+/− craniosynostosis. Conclusions: Our findings suggest an imbalance and/or decrease in resident skeletal stem cells within the cranial sutures gives rise to craniosynostosis, however, restoring this representation by enriching skeletal stem cells within the suture can maintain patency.

2020-04-15 | GSE138881 | GEO

Skeletal Stem Cell Powering Cranial Suture Fate: An Answer to Craniosynostosis (bulk_RNA-seq)

2020-04-15 | GSE138880 | GEO

Single Suture Craniosynostosis: Gene and Pathway Discovery

Project description:Single Suture Craniosynostosis: Gene and Pathway Discovery

| PRJNA776387 | ENA

Single Suture Craniosynostosis: Gene and Pathway Discovery

Project description:Single Suture Craniosynostosis: Gene and Pathway Discovery

| PRJNA776389 | ENA

Calvarial osteoblast transcriptome analysis identifies genetic targets and extracellular matrix-mediated focal adhesion as potential biomarkers for single-suture craniosynostosis

Project description:Craniosynostosis is a disease defined by premature fusion of one or more cranial sutures. The mechanistic pathology of isolated single-suture craniosynostosis is complex and while a number of genetic biomarkers and environmental predispositions have been identified, in many cases the causes remain controversial and inconclusive at best. After controlling for variables contributing to potential bias, FGF7, SFRP4, and VCAM1 emerged as potential genetic biomarkers for single-suture craniosynostosis due to their significantly large changes in gene expression compared to the control population. Furthermore, pathway analysis implicated focal adhesion and extracellular matrix (ECM)-receptor interaction as differentially regulated gene networks when comparing all cases of single-suture synostosis and controls. Lastly, overall gene expression was found to be highly conserved between coronal and metopic cases, as evidenced by the fact that WNT2 and IGFBP2 were the only differentially regulated genes identified in a direct comparison. These results not only confirm the roles of previously reported craniosynostosis-related targets but also introduce novel genetic biomarkers and pathways that may play critical roles in its pathogenesis.

2012-03-04 | GSE27976 | GEO

Calvarial osteoblast transcriptome analysis identifies genetic targets and extracellular matrix-mediated focal adhesion as potential biomarkers for single-suture craniosynostosis

2012-03-04 | E-GEOD-27976 | biostudies-arrayexpress