Mus musculus
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA130643 | ENA |
REPOSITORIES: ENA
Similar Datasets
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:Transcription factor FoxQ1 belongs to family of Fox transcription factors containing forkhead box (winged helix) domain. This family of proteins plays an important role in cell growth, proliferation, and differentiation. Expression of FoxQ1 was found in cancer cells and was associated with increased migration and invasion. Recently, elevated FoxQ1 expression was found in IL4 stimulated macrophages. We used microarrays to clarify the role of FoxQ1 in macrophages
2017-11-23 | GSE79521 | GEO
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
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. Keywords: mutant mouse stomach
2008-05-01 | GSE8943 | GEO
Project description:The forkhead box transcription factor FOXQ1 is aberrantly induced in various cancers, and contributes to tumour growth and metastasis. It has been suggested that the oncogenic potential of FOXQ1 may be explained by its activation of the Wnt/β-catenin signalling pathway.However, the mode of action of FOXQ1 in the Wnt pathway remains to be resolved. Here we report that FOXQ1 is bimodal transcriptional activator of Wnt target gene expression in normal and cancer cells. Using co-immunoprecipitation, proximity proteomics, and reporter assays, we show that FOXQ1 engages the Wnt transcriptional complex to promote gene expressionvia TCF/LEF transcription factors.
2022-10-05 | PXD030464 | Pride
Project description:The forkhead box transcription factor FOXQ1 is aberrantly induced in various cancers, and contributes to tumour growth and metastasis. It has been suggested that the oncogenic potential of FOXQ1 may be explained by its activation of the Wnt/β-catenin signalling pathway. However, the mode of action of FOXQ1 in the Wnt pathway remains to be resolved. Here we report that FOXQ1 is bimodal transcriptional regulator of Wnt target gene expression in normal and cancer cells. Using co-immunoprecipitation, proximity proteomics, and reporter assays, we show that FOXQ1 partly engages the Wnt transcriptional complex to promote gene expression via TCF/LEF transcription factors.
2022-10-05 | PXD035624 | Pride
Project description:Numerous epithelial-to-mesenchymal transition (EMT)-promoting transcription factors have been implicated in tumorigenesis or metastasis, as well as chemoresistance of cancer. However, the underlying mechanism mediating these processes is unclear. Here we report that Foxq1, a forkhead box-containing transcription factor and EMT-inducing gene, promotes stemness traits and chemoresistance in mammary epithelial cells. We identify Twist1, Zeb2, and PDGFRα and β as Foxq1 downstream targets using an expression profiling assay. Further studies reveal that PDGFRα and β can be directly regulated by Foxq1, or indirectly through Twist1. Knockdown of both PDGFRα and β shows more significant effects on reversing Foxq1-promoted oncogenesis in vitro and in vivo than knockdown by either PDGFRα or β alone. PDGFRβ, but not PDGFRα, shows potent effects in reversing Foxq1-promoted stemness traits. Moreover, pharmacological inhibition or gene silencing of PDGFRs sensitize mammary epithelial cells to chemotherapeutic agents in vitro and in vivo. These findings collectively indicate PDGFRs as critical mediators underlying breast cancer tumorigenesis and chemoresistance driven by EMT promoting genes, which have potential clinical implications for cancer therapy.
2013-05-11 | GSE46834 | GEO
Project description:Numerous epithelial-to-mesenchymal transition (EMT)-promoting transcription factors have been implicated in tumorigenesis or metastasis, as well as chemoresistance of cancer. However, the underlying mechanism mediating these processes is unclear. Here we report that Foxq1, a forkhead box-containing transcription factor and EMT-inducing gene, promotes stemness traits and chemoresistance in mammary epithelial cells. We identify Twist1, Zeb2, and PDGFRM-NM-1 and M-NM-2 as Foxq1 downstream targets using an expression profiling assay. Further studies reveal that PDGFRM-NM-1 and M-NM-2 can be directly regulated by Foxq1, or indirectly through Twist1. Knockdown of both PDGFRM-NM-1 and M-NM-2 shows more significant effects on reversing Foxq1-promoted oncogenesis in vitro and in vivo than knockdown by either PDGFRM-NM-1 or M-NM-2 alone. PDGFRM-NM-2, but not PDGFRM-NM-1, shows potent effects in reversing Foxq1-promoted stemness traits. Moreover, pharmacological inhibition or gene silencing of PDGFRs sensitize mammary epithelial cells to chemotherapeutic agents in vitro and in vivo. These findings collectively indicate PDGFRs as critical mediators underlying breast cancer tumorigenesis and chemoresistance driven by EMT promoting genes, which have potential clinical implications for cancer therapy. The purpose of these experiments is to investigate the downstream targets of several transcriptional factors including Foxq1 and IRX5. Another purpose is to compare the expression pattern between basal-like breast cancer cells including MDA-MB231, SUM159 and SUM1315.
2013-05-11 | E-GEOD-46834 | biostudies-arrayexpress
Project description:Introgressed variants from other species can be an important source of genetic variation because they may arise rapidly, can include multiple mutations on a single haplotype, and have often been pretested by selection in the species of origin. Although introgressed alleles are generally deleterious, several studies have reported introgression as the source of adaptive alleles-including the rodenticide-resistant variant of Vkorc1 that introgressed from Mus spretus into European populations of Mus musculus domesticus. Here, we conducted bidirectional genome scans to characterize introgressed regions into one wild population of M. spretus from Spain and three wild populations of M. m. domesticus from France, Germany, and Iran. Despite the fact that these species show considerable intrinsic postzygotic reproductive isolation, introgression was observed in all individuals, including in the M. musculus reference genome (GRCm38). Mus spretus individuals had a greater proportion of introgression compared with M. m. domesticus, and within M. m. domesticus, the proportion of introgression decreased with geographic distance from the area of sympatry. Introgression was observed on all autosomes for both species, but not on the X-chromosome in M. m. domesticus, consistent with known X-linked hybrid sterility and inviability genes that have been mapped to the M. spretus X-chromosome. Tract lengths were generally short with a few outliers of up to 2.7 Mb. Interestingly, the longest introgressed tracts were in olfactory receptor regions, and introgressed tracts were significantly enriched for olfactory receptor genes in both species, suggesting that introgression may be a source of functional novelty even between species with high barriers to gene flow.
| S-EPMC8784167 | biostudies-literature