Gli1-expressing cells form the essential niche for colon stem cells and serve as a reserve Wnt-source in the small intestine
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ABSTRACT:
PROVIDER: PRJNA450092 | ENA |
REPOSITORIES: ENA
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Project description:Purpose: to determine cellular heterogeneity of mesenchymal Gli1-positive cells from colon using single cell RNAse (10xGenomics); Summary: We determined 8 disctinct sub-populations of mesenchymal cells, remaining non-Gli1 epithelial cells formed a distinct separete cluster serving as a internal control of the single cells sequencing procedure
2018-04-17 | GSE113043 | GEO
Project description:Repair-supportive mesenchymal cells (RSMCs) have been recently reported in the context of naphthalene (NA)-induced airway injury and regeneration. These cells transiently express smooth muscle actin (Acta2) and are enriched with platelet-derived growth factor receptor alpha (Pdgfra) and fibroblast growth factor 10 (Fgf10) expression. Genetic deletion of Ctnnb1 (gene coding for beta catenin) or Fgf10 in these cells using the Acta2-Cre-ERT2 driver line after injury (defined as NA-Tam condition; Tam refers to tamoxifen) led to impaired repair of the airway epithelium. In this study, we demonstrate that RSMCs are mostly captured using the Acta2-Cre-ERT2 driver when labeling occurs after (NA-Tam condition) rather than before injury (Tam-NA condition), and that their expansion occurs mostly between days 3 and 7 following NA treatment. Previous studies have shown that lineage-traced peribronchial GLI1+ cells are transiently amplified after NA injury. Here, we report that Gli1 expression is enriched in RSMCs. Using lineage tracing with Gli1Cre-ERT2 mice combined with genetic inactivation of Fgf10, we show that GLI1+ cells with Fgf10 deletion fail to amplify around the injured airways, thus resulting in impaired airway epithelial repair. Interestingly, Fgf10 expression is not upregulated in GLI1+ cells following NA treatment, suggesting that epithelial repair is mostly due to the increased number of Fgf10-expressing GLI1+ cells. Co-culture of SCGB1A1+ cells with GLI1+ cells isolated from non-injured or injured lungs showed that GLI1+ cells from these two conditions are similarly capable of supporting bronchiolar organoid (or bronchiolosphere) formation. Single-cell RNA sequencing on sorted lineage-labeled cells showed that the RSMC signature resembles that of alveolar fibroblasts. Altogether, our study provides strong evidence for the involvement of mesenchymal progenitors in airway epithelial regeneration and highlights the critical role played by Fgf10-expressing GLI1+ cells in this context.
2022-11-09 | GSE215094 | GEO
Project description:GLI1 is a transcription factor correlated to decreased survival in several cancers. We have identified SMARCA2 as a co-regulator that enhances GLI1-mediated transcriptional activity and functions through the C-terminal transcriptional activation domain of GLI1. Central domains including the ATPase motif of SMARCA2 physically interact with GLI1. Evaluation of DNA density indicates GLI1, like SMARCA2, can increase the DNA accessibility with a preference for sites distal to gene transcription start sites and outside the promoter regions (i.e. enhancers). The putative enhancers where accessibility is decreased by the knock down of GLI1 and SMARCA2 are located cis to genes, such as HHIP, that are regulated by GLI1 and implicated in cancer functions. At the putative enhancer for HHIP, the localization of SMARCA2 is at least partially dependent on GLI1’s presence. Understanding this transcriptional regulation by GLI1 and SMARCA2 through altering chromatin accessibility at enhances can provide additional therapeutic targets for cancers dependent on GLI1.
2020-05-11 | GSE143684 | GEO
Project description:Increased expression of GLI1 is associated with poor prognosis for some breast cancer subtypes. A conditional transgenic GLI1 expressing mouse model, with or without heterozygous deletion of Trp53, was used to generate and study GLI1 induced mammary gland tumours. Tumour tissue was serially orthotopically transplanted for at least 10 generations in NSG mice.
2019-06-30 | E-MTAB-7531 | biostudies-arrayexpress
Project description:To assess if Hedgehog (Hh) responding cells in the skin have a unique expression profile, isolated keratinocytes that express the Hh response gene Gli1 were collected by FACS and their gene expression was compared to sorted CD34-expressing cells from the middle bulge region of the hair follicle and to cells from the interfollicular epidermis (IFE) by hybridization of isolated RNA to gene expression microarrays. Dissociated keratinocytes isolated form back skin of Gli1-eGFP/+ mice (2 mice pooled for each replicate) in adult telogen were sorted based on GFP expression and immunostaining for CD34. Only viable, single cells with immunostaining for α6 Integrin (to mark basal keratinocytes) were collected. GFP(+) cells were collected as the Gli1 cohort. GFP(-) CD34(+) cells were collected as the CD34 cohort, and GFP(-) CD34(-) cells were collected as interfollicular epidermis (IFE) cohort. Total RNA was extracted from each cell population and labeled for hybridization to gene expression microarrays. The experiment was preformed in triplicate, however RNA from the Gli1(+) cells in one replicate was of insufficient quality to analyze. For staining of isolated keratinocytes, cells were incubated on ice for 1 hour in SMEM containing 1%BSA and 15μL of anti-CD49f-PE antibody (BDBioscience) plus 5μL anti-CD34-APC antibody (eBioscience) for each 100μL total volume for each 2 million cells. Immediately prior to sorting, DAPI (Invitrogen) was added to the washed cells at 1μg/mL final concentration.
2011-12-01 | E-GEOD-28108 | biostudies-arrayexpress
Project description:To clarify transcriptional target genes of GLI1 in human mammary epithelial cells and breast cancer cells, primary culture cells of human mammary epithelium HMEC and breast cancer cell line MCF-7 were lentivirally transduced by either GLI1 or its control LacZ. Their RNA samples were served for expression analysis using AGILENT human 8x60K cDNA microarray. Array analysis of HMEC and MCF-7 expressing either GLI1 or LacZ. 1 color method was employed.
2015-04-28 | E-GEOD-64350 | biostudies-arrayexpress
Project description:Panc1 (human pancreatic adenocarcinoma cells) cells were transfected with control siRNA (targeting firefly luciferase, siLuc) or siRNA targeting GLI1 (siGLI1, Pool of four siRNAs). 72h following transfection, RNA was prepared for array analysis.
2012-03-31 | E-MEXP-3379 | biostudies-arrayexpress
Project description:SHH signaling pathway is activated in many type of cancers. However, the role of its activation in particular type of cancer was poorly understood. The GLI family transcription factor GLI1 is the effector of Shh pathway activation and functions as oncogene. Our goal of research is to identify the GLI1 targets in desmoplastic medulloblastomas. We used microarrays to obtain the global gene expression profiles in cells transformed by GLI1 and identified distinct classes of genes by comparing with those of desmoplastic medulloblastomas
2009-03-25 | GSE11987 | GEO
Project description:This goal of this microarray analysis is to determine whether the mesonephros-derived theca cells exhibt a different gene expression profile from that of the whole theca cell population The mesonephros-derived (n=3, Tamoxifen at E12.5, E14.5 and E16.5) and the neonatal ovary-derived Gli1-positive cells (n=3 Tamoxifen at P1-3 via lactating dams), were isolated from the adult ovaries of Gli1-CreERT2; Rosa-LSL-tdTomato mice at 2 months of age and were sorted by FACS
2015-04-28 | E-GEOD-66104 | biostudies-arrayexpress
Project description:GLI1 is a transcription factor correlated to decreased survival in several cancers. We have identified SMARCA2 as a co-regulator that enhances GLI1-mediated transcriptional activity and functions through the C-terminal transcriptional activation domain of GLI1. Central domains including the ATPase motif of SMARCA2 physically interact with GLI1. Evaluation of DNA density indicates GLI1, like SMARCA2, can increase the DNA accessibility with a preference for sites distal to gene transcription start sites and outside the promoter regions (i.e. enhancers). The putative enhancers where accessibility is decreased by the knock down of GLI1 and SMARCA2 are located cis to genes, such as HHIP, that are regulated by GLI1 and implicated in cancer functions. At the putative enhancer for HHIP, the localization of SMARCA2 is at least partially dependent on GLI1’s presence. Understanding this transcriptional regulation by GLI1 and SMARCA2 through altering chromatin accessibility at enhances can provide additional therapeutic targets for cancers dependent on GLI1.
2020-05-11 | GSE143681 | GEO