Genome-wide identification of Foxf2 transcriptional target genes in palate development
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ABSTRACT:
PROVIDER: PRJNA565970 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR10132997.fastq.gz | Fastqsanger.gz | |||
| SRR10132998.fastq.gz | Fastqsanger.gz |
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Project description:Cleft palate is among the most common structural birth defects in humans. Previous studies have shown that mutations in FOXF2 are associated with cleft palate in humans and mice and that Foxf2 acts in a Shh-Foxf-Fgf18-Shh molecular network controlling palatal shelf growth. In this study, we generated mice carrying 3xFLAG epitope-tagged endogenous Foxf2 protein using the CRISPR/Cas9-mediated genome editing technology and characterized genome-wide Foxf2 binding sites in the developing palatal shelves using chromatin immunoprecipitation and genome sequencing (ChIP-seq). By combined analysis of ChIP-seq and RNA-seq datasets we identified a large list of Foxf2 target genes. Further analyses demonstrate that Foxf2 directly regulate expression of several genes encoding ECM or ECM modifiers during palate development. Moreover, our ChIP-seq and RNA-seq datasets provide an excellent resource for comprehensive understanding of the molecular network controlling palate development.
2020-02-11 | GSE137585 | GEO
Project description:Cleft palate is among the most common structural birth defects in humans. Previous studies have shown that mutations in FOXF2 are associated with cleft palate in humans and mice and that Foxf2 acts in a Shh-Foxf-Fgf18-Shh molecular network controlling palatal shelf growth. In this study, we combined RNA-seq and ChIP-seq approaches to identify direct transcriptional target genes mediating Foxf2 function in palate development in mice. Of 155 genes that exhibited Foxf2-dependent expression in the developing palatal mesenchyme, 88 contained or were located next to Foxf2-binding sites. Through in situ hybridization analyses, we demonstrate that expression of many of these target genes, including multiple genes encoding transcription factors and several encoding extracellular matrix-modifying proteins, were specifically upregulated in the posterior region of palatal shelves in Foxf2-/- mouse embryos. Foxf2 occupancy at many of these putative target loci, including Fgf18, in the developing palatal tissues was verified by ChIP-polymerase chain reaction analyses. One of the Foxf2 target genes, Chst2, encodes a carbohydrate sulfotransferase integral to glycosaminoglycan sulfation. Correlating with ectopic Chst2 expression, Foxf2-/- embryos a exhibited region-specific increase in sulfated keratan sulfate and a concomitant reduction in chondroitin sulfate accumulation in the posterior palatal mesenchyme. However, expression of the core protein of versican, a major chondroitin sulfate proteoglycan important in palatal shelf morphogenesis, was increased, whereas expression of collagen I was reduced in the corresponding region of the palatal mesenchyme. These results indicate that, in addition to regulating palatal shelf growth through the Fgf18-Shh signaling network, Foxf2 controls palatal shelf morphogenesis through regulating expression of multiple transcription factors as well as through directly controlling the synthesis and processing of extracellular matrix components in the palatal mesenchyme. Our ChIP-seq and RNA-seq data sets provide an excellent resource for comprehensive understanding of the molecular network controlling palate development.
| S-EPMC7088206 | biostudies-literature
Project description:The tongue is a specialized muscular organ that performs multiple essential functions including mastication, deglutition, oral sensation, oral cleansing, airway maintenance and vocalization. In this study, we show Foxf1/Foxf2 serves as key mediators of hedgehog signaling in regulating myoblast migration, differentiation, and intrinsic tongue muscle organization. We took advantage of the Foxf2FLAG mice which carries 3xFLAG epitope-tagged endogenous Foxf2 protein and characterized genome-wide Foxf2 binding sites in the developing tongues using chromatin immunoprecipitation and genome sequencing (ChIP-seq). Further analyses demonstrate that Foxf1/2 transcription factors directly control the expression of Hgf, Tgfb2, and Tgfb3, to regulate tongue myogenesis.
2022-10-14 | GSE195788 | GEO
Project description:Genome-wide identification of Foxf2 transcriptional target genes in tongue development
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Project description:This genome-wide gene expression studies are aimed at deciphering whether FOXF2 transcriptional activity and specificity are compromised in FOXF2-expressing breast cancer cells (MDA-MB-231) compared with FOXF2-expressing normal breast epithelial cells (MCF10A).
2017-07-31 | GSE55675 | GEO
Project description:To identify the genes and pathways regulated by FOXF2, we investigated potential FOXF2 gene targets by microarray analyses of primary prostate stromal cells (PrSC) in which FOXF2 was knocked down by siRNA. 190 differentially expressed genes were selected, of which 104 genes were more highly expressed in PrSC cells treated with FOXF2 siRNA and 86 were more highly expressed in PRSC cells treated with negative control siRNA.
2008-11-01 | GSE12444 | GEO
Project description:Previous studies have identified the odd-skipped related 2 (Osr2) transcription factor as a key intrinsic regulator of palatal shelf growth and morphogenesis. However, little is known about the molecular program acting downstream of Osr2 in the regulation of palatogenesis. In this study, we isolated palatal mesenchyme cells from embryonic day 12.5 (E12.5) and E13.5 Osr2RFP/+ and Osr2RFP/- mutant mouse embryos and performed whole transcriptome RNA sequencing analyses. Differential expression analysis of the RNA sequencing datasets revealed that expression of 70 genes was upregulated and expression of 61 genes was downregulated by >1.5-fold at both E12.5 and E13.5 in the Osr2RFP/- palatal mesenchyme cells, in comparison with Osr2RFP/+ littermates. Gene ontology analysis revealed enrichment of signaling molecules and transcription factors crucial for skeletal development and osteoblast differentiation among those significantly upregulated in the Osr2 mutant palatal mesenchyme. Using quantitative real-time polymerase chain reaction (RT-PCR)and in situ hybridization assays, we validated that the Osr2-/- embryos exhibit significantly increased and expanded expression of many osteogenic pathway genes, including Bmp3, Bmp5, Bmp7, Mef2c, Sox6, and Sp7 in the developing palatal mesenchyme. Furthermore, we demonstrate that expression of Sema3a, Sema3d, and Sema3e, is ectopically activated in the developing palatal mesenchyme in Osr2-/- embryos. Through chromatin immunoprecipitation, followed by RT-PCR analysis, we demonstrate that endogenous Osr2 protein binds to the promoter regions of the Sema3a and Sema3d genes in the embryonic palatal mesenchyme. Moreover, Osr2 expression repressed the transcription from the Sema3a and Sema3d promoters in cotransfected cells. Since the Sema3 subfamily of signaling molecules plays diverse roles in the regulation of cell proliferation, migration, and differentiation, these data reveal a novel role for Osr2 in regulation of palatal morphogenesis through preventing aberrant activation of Sema3 signaling. Together, these data indicate that Osr2 controls multiple molecular pathways, including BMP and Sema3 signaling, in palate development.
| S-EPMC5652858 | biostudies-literature
Project description:Background: The FACEBASE consortium was established in part to create a central resource for craniofacial researchers. One purpose is to provide a molecular anatomy of craniofacial development. To this end we have used a combination of laser capture microdissection and RNA-Seq to define the gene expression programs driving development of the murine palate. Results: We focused on the E14.5 palate, soon after medial fusion of the two palatal shelves. The palate was divided into multiple compartments, including medial and lateral, as well as oral and nasal, for both the anterior and posterior domains. A total of 25 RNA-Seq datasets were generated. The results provide a comprehensive view of the region specific expression of all transcription factors, growth factors and receptors. Paracrine interactions can be inferred from flanking compartment growth factor/receptor expression patterns. The results are validated primarily through very high concordance with extensive previously published gene expression data for the developing palate. In addition selected immunostain validations were carried out. Conclusions: This report provides an RNA-Seq based atlas of gene expression patterns driving palate development at microanatomic resolution. This FACEBASE resource is designed to fuel discovery by the craniofacial research community. Laser capture microdissection and RNA-seq were used to generate gene expression profiles of different compartments of the mouse E14.5 developing palate
2015-04-03 | E-GEOD-67525 | biostudies-arrayexpress
Project description:To identify the genes and pathways regulated by FOXF2, we investigated potential FOXF2 gene targets by microarray analyses of primary prostate stromal cells (PrSC) in which FOXF2 was knocked down by siRNA. 190 differentially expressed genes were selected, of which 104 genes were more highly expressed in PrSC cells treated with FOXF2 siRNA and 86 were more highly expressed in PRSC cells treated with negative control siRNA. Experiment Overall Design: In each experiment, we compared gene expression of PrSC cells treated with FOXF2 siRNA versus PrSC cells treated with negative control siRNA, in a total of 6 affymetrix arrays. 190 differentially expressed genes were selected (ratio negative control siRNA/siRNA ⥠2log |0.8| as average in all arrays).
2008-11-13 | E-GEOD-12444 | biostudies-arrayexpress
Project description:Brain of the foxf2 mutant mouse embryo shows microvascular aneurysm, underdeveloped blood brain barrier and also significant defects in the tissue integrity. Foxf2 expresses in the pericytes of the brain and seem to play an important role in proper development of the BBB. Brains of E18.5 wt and foxf2 mutant mouse embryos dissected and RNA extracted from the brains using Sigma mammalian total RNA extraction kit. The RNA then been sent to th core facility for hybridization.
2015-03-02 | E-GEOD-54531 | biostudies-arrayexpress