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Transcriptome and chromatin accessiblity analysis of mice soft palate to unreveal the role of Runx2 in regulating palate muscle development.

ABSTRACT: Transcriptome and chromatin accessiblity analysis of mice soft palate to unreveal the role of Runx2 in regulating palate muscle development.

PROVIDER: PRJNA656132 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR12416691.fastq.gz	Fastqsanger.gz
	SRR12416692.fastq.gz	Fastqsanger.gz
	SRR14130122.fastq.gz	Fastqsanger.gz
	SRR14130123.fastq.gz	Fastqsanger.gz
	SRR14130124.fastq.gz	Fastqsanger.gz

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Transcriptome and chromatin accessiblity analysis of mice soft palate to unreveal the role of Runx2 in regulating palate muscle development.

Project description:We report the application of single cell transcriptome, bulk transcriptome, and chromatin accessibility analysis for investigating the role of Runx2 in regulating soft palate muscle development. By isolating single cells from soft palate tissue of wild type embryos at E13.5, E14.5 and E15.5, we describe the heterogeneity of soft palate mesenchyme during development by analyzing single cell transcriptome. Combined analysis of bulk and single cell transcriptome of soft palate from wild type and Runx2 mutant suggests Runx2 activate expression of perimysial markers. Finally, we show that Runx2 activates expression of perimysial markers probably by repressing Twist1 through chromatin accessibility analysis. This study provides the first single cell level heterogeneity analysis of developing soft palate and shows the important role of Runx2 in regulating soft palate muscle development.

2021-01-27 | GSE155928 | GEO

Comparison of microRNA expression profiles in soft palate muscle of patients with OSAHS and chronic tonsillitis.

Project description:The expression profile of miRNAs in soft palate muscle of patients with OSAHS (obstructive sleep apnea/hypopnea syndrome) and chronic tonsillitis was examined using miRNA microarray analysis. Combining with the following real time PCR and bioinformatics analysis, the physiological importance of the miRNA-autophagy interconnection is far more likely to be elucidated.

2019-09-25 | GSE99239 | GEO

Proteogenomics uncovers critical elements of host response in bovine soft palate epithelial cells following in vitro infection with foot-and-mouth disease virus (FMDV)

Project description:The pathogen and host factors that contribute to the establishment of foot-and-mouth disease virus (FMDV) persistence are currently not understood. Using primary bovine soft palate multilayers in combination with RNA sequencing, we analyzed the transcriptional responses during acute and persistent FMDV infection.

2019-01-18 | E-MTAB-7605 | biostudies-arrayexpress

Proteogenomics uncovers critical elements of host response in bovine soft palate epithelial cells following in vitro infection with foot-and-mouth disease virus (FMDV)

Project description:: Foot-and-mouth disease (FMD) is the most devastating disease of cloven-hoofed livestock, with a crippling economic burden in endemic areas and immense costs associated with outbreaks in free countries. Foot-and-mouth disease virus (FMDV), a picornavirus, will spread rapidly in naïve populations, reaching morbidity rates of up to 100% in cattle. Even after recovery, over 50% of cattle remain subclinically infected and infectious virus can be recovered from the nasopharynx. The pathogen and host factors that contribute to FMDV persistence are currently not understood. Using for the first time primary bovine soft palate multilayers in combination with proteogenomics, we analyzed the transcriptional responses during acute and persistent FMDV infection. During the acute phase viral RNA and protein was detectable in large quantities and in response hundreds of interferon-stimulated genes (ISG) were overexpressed, mediating antiviral activity and apoptosis. Although the number of pro-apoptotic ISGs and the extent of their regulation decreased during persistence, some ISGs with antiviral activity were still highly expressed at that stage. This indicates a long-lasting but ultimately ineffective stimulation of ISGs during FMDV persistence. Furthermore, downregulation of relevant genes suggests an interference with the extracellular matrix that may contribute to the skewed virus-host equilibrium in soft palate epithelial cells.

2019-01-17 | PXD012242 | Pride

Genome-wide Runx2 occupancy in prostate cancer cells suggests a role in regulating secretion.

Project description:Runx2 is a metastatic transcription factor (TF) increasingly expressed during prostate cancer (PCa) progression. Using PCa cells conditionally expressing Runx2, we previously identified Runx2-regulated genes with known roles in epithelial-mesenchymal transition, invasiveness, angiogenesis, extracellular matrix proteolysis and osteolysis. To map Runx2-occupied regions (R2ORs) in PCa cells, we first analyzed regions predicted to bind Runx2 based on the expression data, and found that recruitment to sites upstream of the KLK2 and CSF2 genes was cyclical over time. Genome-wide ChIP-seq analysis at a time of maximum occupancy at these sites revealed 1,603 high-confidence R2ORs, enriched with cognate motifs for RUNX, GATA and ETS TFs. The R2ORs were distributed with little regard to annotated transcription start sites (TSSs), mainly in introns and intergenic regions. Runx2-upregulated genes, however, displayed enrichment for R2ORs within 40 kb of their TSSs. The main annotated functions enriched in 98 Runx2-upregulated genes with nearby R2ORs were related to invasiveness and membrane trafficking/secretion. Indeed, using SDS-PAGE, mass spectrometry and western analyses, we show that Runx2 enhances secretion of several proteins, including fatty acid synthase and metastasis-associated laminins. Thus, combined analysis of Runx2’s transcriptome and genomic occupancy in PCa cells lead to defining its novel role in regulating protein secretion. Examination of Runx2 in Prostate Cancer cells

2011-11-29 | E-GEOD-33889 | biostudies-arrayexpress

Tamoxifen induces cleft palate in mice

Project description:Tamoxifen (TAM), a widely-used drug in treating breast cancer, has been reported to be associated with craniofacial defects including micrognathia and cleft palate in humans. However, the exact effects of TAM on the developing palate remain unclear. In the present study, we conclude that excess TAM exposure causes cleft palate defect in mice by regulating MAPK pathways, which implicates the importance of tightly regulated MAPK signaling in palate development and provides a basis for further exploration of the molecular etiology of cleft palate defects caused by environmental factors.

2022-11-22 | GSE140836 | GEO

Genome-wide Runx2 occupancy in prostate cancer cells suggests a role in regulating secretion.

2011-11-29 | GSE33889 | GEO

Runx2-Twist1 interaction coordinates cranial neural crest guidance of soft palate myogenesis.

Project description:Cranial neural crest (CNC) cells give rise to bone, cartilage, tendons, and ligaments of the vertebrate craniofacial musculoskeletal complex, as well as regulate mesoderm-derived craniofacial muscle development through cell-cell interactions. Using the mouse soft palate as a model, we performed an unbiased single-cell RNA-seq analysis to investigate the heterogeneity and lineage commitment of CNC derivatives during craniofacial muscle development. We show that Runx2, a known osteogenic regulator, is expressed in the CNC-derived perimysial and progenitor populations. Loss of Runx2 in CNC-derivatives results in reduced expression of perimysial markers (Aldh1a2 and Hic1) as well as soft palate muscle defects in Osr2-Cre;Runx2fl/fl mice. We further reveal that Runx2 maintains perimysial marker expression through suppressing Twist1, and that myogenesis is restored in Osr2-Cre;Runx2fl/fl;Twist1fl/+ mice. Collectively, our findings highlight the roles of Runx2, Twist1, and their interaction in regulating the fate of CNC-derived cells as they guide craniofacial muscle development through cell-cell interactions.

| S-EPMC7826157 | biostudies-literature

Gene expression profiling of the palate in Erk2 mutant mouse models

2015-12-11 | GSE67087 | GEO

Gene expression profiling of the palate in Erk2 mutant mouse models

Project description:The overall goal of this project is to investigate the role of Erk2-mediated signaling in regulating the cellular metabolism of cranial neural crest (CNC) cells during palate development. Here, we conducted gene expression profiling of palate tissue from wild type mice as well as those with a neural crest specific conditional inactivation of the Erk2 gene. The latter mice exhibit micrognathia, tongue defects and cleft palate, which is among the most common congenital birth defects and observed in many syndromic conditions. To investigate the adverse effects of dysfunctional ERK signaling on the cellular metabolism of palatal mesenchyme during palatogenesis, we analyzed mice with a neural crest cell-specific conditional inactivation of Erk2 (Erk2fl/fl;Wnt1-Cre). We performed microarray analyses of primary mouse embryonic palatal mesenchymal cells of Erk2fl/fl;Wnt1-Cre mutant mice and Erk2fl/fl control mice, collected at embryonic day 13.5 (n=3 per genotype) and E14.5 (n=5 per genotype).

2015-12-11 | E-GEOD-67087 | biostudies-arrayexpress

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