FOXQ1 Regulates Mitochondrial Cristae Formation and Energy Metabolism in Mouse Brain Endothelial Cells [CUT&TAG]
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ABSTRACT:
ORGANISM(S): Mus musculus
PROVIDER: GSE271829 | GEO | 2024/07/16
REPOSITORIES: GEO
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Project description:Purpose: To gain futher insight into how FOXQ1 regulates the brain endothelial cells ,RNA-seq was used to analyze the genome-wide changes resulting from the cerebral cortical endothelial cells of E18 FOXQ1 conditional knock out mice and littermate wild-type. Methods: Total RNA from E18 Flow sorting of endothelial cells of wild-type(WT) and FOXQ1fl/fl;Tie2-Cre mice was extracted. Specifically, Agilent 2100 Bioanalyze was used to quality controlled and quantified. then, total RNA was converted to cDNA and bound the library. RNA-sequencing analysis was used by the Illumina HiSeq 6000 platform in Annoroad Genomics Approximately one thousand transcripts showed differential expression between the wild-type(WT) and FOXQ1fl/fl;Tie2-Cre mice cortical endothelial cells, with a fold change ≥1.5 and p value <0.05. These results reflected FOXQ1 plays a role in brain endothelial cells. Conclusions: RNA-seq based transcriptome characterization would provide a overall understanding how FOXQ1 works in endothelial cells.
2024-07-16 | GSE271827 | GEO
Project description:FOXQ1 Regulates Mitochondrial Cristae Formation and Energy Metabolism in Mouse Brain Endothelial Cells [CUT&TAG]
| PRJNA1133709 | ENA
Project description:FOXQ1 Regulates Mitochondrial Cristae Formation and Energy Metabolism in Mouse Brain Endothelial Cells [RNA-seq]
| PRJNA1133705 | ENA
Project description:The transcriptional mechanisms coordinating angiogenic sprouting with the acquisition of barrier properties in the developing central nervous system (CNS) remain incompletely defined. Here, we demonstrate that the forkhead box transcription factor Foxq1 is essential for CNS angiogenesis and blood-brain barrier (BBB) formation. Endothelial-specific deletion of Foxq1 in mice resulted in defective angiogenesis in the brain and retina, characterized by impaired tip cell identity, reduced vascular coverage, and diminished proliferation. Moreover, mutant embryos exhibited compromised BBB integrity, evidenced by enhanced leakage of molecular tracers. Single-cell transcriptomics revealed that Foxq1 is enriched in tip cells and barrier-competent capillary populations, and its loss disrupts the transcriptional programs governing both endothelial sprouting and barrier maturation. Mechanistically, Foxq1 couples angiogenic morphogenesis with BBB acquisition by regulating tip cell-enriched transcripts such as Esm1, alongside core barrier determinants including Cdh5 and Mfsd2a.These findings establish Foxq1 as a critical transcriptional link between CNS vascular growth and functional barrier establishment, with implications for understanding neurovascular developmental disorders.
2026-06-01 | GSE332948 | GEO
Project description:The Forkhead family of transcription factors comprises numerous members and is implicated in various cellular functions, including cell growth, apoptosis, migration and differentiation.In this study we identified the Forkhead factor FoxQ1 as increased in expression during TGF-beta1 induced changes in epithelial differentiation, suggesting functional roles of FoxQ1 for epithelial plasticity.The repression of FoxQ1 in mammary epithelial cells led to a change in cell morphology characterized by an increase in cell size, pronounced cell-cell contacts and an increased expression of several junction proteins (e.g. E-cadherin). In addition, FoxQ1 knock-down cells revealed rearrangements in the actin-cytoskeleton and slowed down cell cycle G1-phase progression.Furthermore, repression of FoxQ1 enhanced the migratory capacity of coherent mammary epithelial cells.Gene expression profiling of NM18 cells indicated that FoxQ1 is a relevant downstream mediator of TGF-beta1 induced gene expression changes. This included the differential expression of transcription factors involved in epithelial plasticity, e.g. Ets-1, Zeb1 and Zeb2.In summary, this study has elucidated the functional impact of FoxQ1 on epithelial differentiation
2010-09-01 | GSE23833 | GEO
Project description:FOXQ1 is a putative oncogene in several types of carcinomas and, in colorectal cancers, is one of the most highly upregulated genes. FOXQ1 has been previously identified as a candidate Wnt pathway activator in CRC cells. However, it is still unclear how the crosstalk between FOXQ1 and Wnt signalling influence the global behaviour of colorectal cancer cells. Here, we performed bulk RNA sequencing of FOXQ1 or vector transfected HCT116 cells with or without Wnt3a treatment. Each condition was performed in biological triplicates.
2022-09-23 | E-MTAB-12062 | biostudies-arrayexpress
Project description:We report the genome wide RNA sequencing for high-throughput profiling of FOXQ1 target genes in melanoma and carcinoma cells. We generated melanoma (SK-Mel-147) and ovarian carcinoma cells (SCOV3) ectopically expressing FOXQ1. We find that FOXQ1 differentially regulates the expression of several genes in melanoma cells as compared to carcinoma cells. Specifically, FOXQ1 induces the expression of several genes in ovarian carcinoma cells SCOV3 and suppresses the expression of the same genes in melanom cells. We show that this differentialy regulation of the same target gene depends upon the nuclear levels of beta-catenin. High levels of active nuclear beta-catenin promote FOXQ1 mediated transcriptional activation of genes whereas low levels contribute to TLE/Groucho- mediated repression. This study provides a framework for understanding the lineage specific pattern of transcriptional regulation by FOXQ1 and its contextual determinants.
2017-08-25 | GSE103071 | GEO
Project description:The Forkhead family of transcription factors comprises numerous members and is implicated in various cellular functions, including cell growth, apoptosis, migration and differentiation.In this study we identified the Forkhead factor FoxQ1 as increased in expression during TGF-beta1 induced changes in epithelial differentiation, suggesting functional roles of FoxQ1 for epithelial plasticity.The repression of FoxQ1 in mammary epithelial cells led to a change in cell morphology characterized by an increase in cell size, pronounced cell-cell contacts and an increased expression of several junction proteins (e.g. E-cadherin). In addition, FoxQ1 knock-down cells revealed rearrangements in the actin-cytoskeleton and slowed down cell cycle G1-phase progression.Furthermore, repression of FoxQ1 enhanced the migratory capacity of coherent mammary epithelial cells.Gene expression profiling of NM18 cells indicated that FoxQ1 is a relevant downstream mediator of TGF-beta1 induced gene expression changes. This included the differential expression of transcription factors involved in epithelial plasticity, e.g. Ets-1, Zeb1 and Zeb2.In summary, this study has elucidated the functional impact of FoxQ1 on epithelial differentiation Cells treated with 200µM 4sU for 2h, biological replicate 1:2h_co._total1, Cells treated with 200µM 4sU for 2h, biological replicate 2:2h_co._total2, Cells treated with 200µM 4sU for 2h, biological replicate 3 :2h_co._total3, Cells treated with 200µM 4sU for 2h and enriched for 4sU labelled RNA, biological replicate 1: 2h_co._enriched1, Cells treated with 200µM 4sU for 2h and enriched for 4sU labelled RNA, biological replicate 2: 2h_co._enriched2, Cells treated with 200µM 4sU for 2h and enriched for 4sU labelled RNA, biological replicate 3:2h_co._enriched3, Cells treated with 5 ng/ml TGF-b1 and 200µM 4sU for 2h, biological replicate 1:2h_TGFbeta_total1, Cells treated with 5 ng/ml TGF-b1 and 200µM 4sU for 2h, biological replicate 2:2h_TGFbeta_total2, Cells treated with 5 ng/ml TGF-b1 and 200µM 4sU for 2h, biological replicate 3:2h_TGFbeta_total3, Cells treated with 5 ng/ml TGF-b1 and 200µM 4sU for 2h and enriched for 4sU labelled RNA, biological replicate 1:2h_TGFbeta_enriched1, Cells treated with 5 ng/ml TGF-b1 and 200µM 4sU for 2h and enriched for 4sU labelled RNA, biological replicate 2:2h_TGFbeta_enriched2, Cells treated with 5 ng/ml TGF-b1 and 200µM 4sU for 2h and enriched for 4sU labelled RNA, biological replicate 3:2h_TGFbeta_enriched3, FoxQ1 dataset Cells transfected with 25nm scrambled siRNA for 48hrs, biological replicate 1:ns-siRNA 48hrs 1, Cells transfected with 25nm scrambled siRNA for 48hrs, biological replicate 2:ns-siRNA 48hrs 2, Cells transfected with 25nm scrambled siRNA for 48hrs, biological replicate 3:ns-siRNA 48hrs 3, Cells transfected with 25nm scrambled siRNA for 48hrs and treated with TGF-b1 for 40hrs biological replicate 1:ns-siRNA 48hrs TGF-b1 40hrs 1, Cells transfected with 25nm scrambled siRNA for 48hrs and treated with TGF-b1 for 40hrs biological replicate 2:ns-siRNA 48hrs TGF-b1 40hrs 2, Cells transfected with 25nm scrambled siRNA for 48hrs and treated with TGF-b1 for 40hrs biological replicate 3:ns-siRNA 48hrs TGF-b1 40hrs 3, Cells transfected with 25nm FoxQ1 siRNA for 48hrs and treated with TGF-b1 for 40hrs biological replicate 1:FoxQ1 siRNA 48hrs TGF-b1 40hrs 1, Cells transfected with 25nm FoxQ1 siRNA for 48hrs and treated with TGF-b1 for 40hrs biological replicate 2:FoxQ1 siRNA 48hrs TGF-b1 40hrs 2 Cells transfected with 25nm FoxQ1 siRNA for 48hrs and treated with TGF-b1 for 40hrs biological replicate 3:FoxQ1 siRNA 48hrs TGF-b1 40hrs 3
2010-09-01 | E-GEOD-23833 | biostudies-arrayexpress
Project description:Transcription factor Foxq1 controls mucin gene expression and granule content in mouse stomach surface mucous cells ; Background and Aims: The gastric mucosa provides a stringent epithelial barrier and produces acid and enzymes that initiate digestion. In this regenerating tissue, progenitors differentiate continually into 4 principal specialized cell types, yet underlying mechanisms of differentiation are poorly understood. We identified stomach-restricted expression of the forkhead transcription factor FOXQ1. Methods: We used a combination of genetic, histochemical, ultrastructural and molecular analysis to study gastric cell lineages with respect to FOXQ1. Results: Within the developing and adult gastrointestinal tract, Foxq1 mRNA is restricted to the stomach, expressed prominently in foveolar (pit) cells, the abundant mucin-producing cells that line the mucosal surface, and required for their complete differentiation. Mice carrying Foxq1 coding mutations show virtual absence of mRNA and protein for the backbone of the predominant stomach mucin, MUC5AC. These observations correspond to a paucity of foveolar-cell secretory vesicles and notable loss of stomach but not intestinal mucus. Transcriptional profiling identified a surprisingly restricted set of genes with altered expression in Foxq1 mutant stomachs. MUC5AC is a highly tissue-restricted product that similarly depends on FOXQ1 in its other major site of expression, conjunctival goblet cells. Conclusions: Taken together, these observations imply that promotion of gastric MUC5AC synthesis is a primary, cell-autonomous function of FOXQ1. This study is the first to implicate a transcription factor in terminal differentiation of foveolar cells and begins to define the requirements to assemble highly specialized organelles and cells in the gastric mucosa. DOI: 10.1053/j.gastro.2008.04.019 Experiment Overall Design: RNA from stomach antrum from 2 of each Satin, Beige, and BL6 mice were compared using microarray analysis.
2008-06-16 | E-GEOD-8943 | biostudies-arrayexpress