Protein Syndesmos is a novel RNA binding protein that regulates primary cilia formation [Illumina array]
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ABSTRACT:
PROVIDER: PRJNA484186 | ENA |
REPOSITORIES: ENA
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Project description:Protein Syndesmos is a novel RNA binding protein that regulates primary cilia formation
| PRJNA484184 | ENA
Project description:Protein Syndesmos is a novel RNA binding protein that regulates primary cilia formation [Ribo-seq]
| PRJNA484185 | ENA
Project description:Protein Syndesmos is a novel RNA binding protein that regulates primary cilia formation [iCLIP-seq]
| PRJNA484188 | ENA
Project description:Primary cilia play critical roles in sensory and signaling functions, and their dysregulation is associated with developmental abnormalities and multi-organ diseases. Despite their importance, the transcriptional regulation of primary cilia genes is unclear. Here, we employed transcriptome and mouse genetic tools to identify a master regulator of primary cilia genes. By comparing ciliated and non-ciliated cells in the early embryo using scRNA-seq and ChIP-seq, we uncovered that a wide spectrum of primary cilia genes are upregulated in ciliated cells and that SP5/8 within the SP/KLF family of transcription factors bind a core set of cilia genes. Loss- and gain-of-function assays in mouse embryos and embryonic stem cells demonstrate Sp5/8, are required for the initial formation of primary cilia in all embryonic cell types. Moreover, Sp5/8 loss compromises the formation of the more specialized motile cilia present in the embryonic node. Finally, misexpression of SP8 is sufficient to induce primary cilia formation in two unciliated cell types. Our findings demonstrate that SP5/8 are essential for cilia initiation in the embryo and sufficient to drive cilia formation in unciliated cells.
2025-06-25 | GSE274844 | GEO
Project description:Primary cilia play critical roles in sensory and signaling functions, and their dysregulation is associated with developmental abnormalities and multi-organ diseases. Despite their importance, the transcriptional regulation of primary cilia genes is unclear. Here, we employed transcriptome and mouse genetic tools to identify a master regulator of primary cilia genes. By comparing ciliated and non-ciliated cells in the early embryo using scRNA-seq and ChIP-seq, we uncovered that a wide spectrum of primary cilia genes are upregulated in ciliated cells and that SP5/8 within the SP/KLF family of transcription factors bind a core set of cilia genes. Loss- and gain-of-function assays in mouse embryos and embryonic stem cells demonstrate Sp5/8, are required for the initial formation of primary cilia in all embryonic cell types. Moreover, Sp5/8 loss compromises the formation of the more specialized motile cilia present in the embryonic node. Finally, misexpression of SP8 is sufficient to induce primary cilia formation in two unciliated cell types. Our findings demonstrate that SP5/8 are essential for cilia initiation in the embryo and sufficient to drive cilia formation in unciliated cells.
2025-06-25 | GSE293888 | GEO
Project description:We show here that SDOS interacts with another important cancer-linked protein, the chaperone TRAP1, associates with actively translating polyribosomes and represses translation. Moreover, we demonstrate that SDOS binds directly RNA in living cells. Combining individual gene expression profiling, nucleotide cross-linking and immunoprecipitation (iCLIP), and ribosome profiling, we discover several crucial pathways regulated post-transcriptionally by SDOS.
2018-09-26 | GSE118035 | GEO
Project description:Primary cilia play critical roles in sensory and signaling functions, and their dysregulation is associated with developmental abnormalities and multi-organ diseases1,2. Despite their importance, the transcriptional regulation of primary cilia genes is unclear. Here, we employed transcriptome and mouse genetic tools to identify a master regulator of primary cilia genes. By comparing ciliated and non-ciliated cells in the early embryo using scRNA-seq and ChIP-seq, we uncovered that a wide spectrum of primary cilia genes are upregulated in ciliated cells and that SP5/8 within the SP/KLF family of transcription factors bind a core set of cilia genes. Loss- and gain-of-function assays in mouse embryos and embryonic stem cells demonstrate Sp5/8, are required for the initial formation of primary cilia in all embryonic cell types. Moreover, Sp5/8 loss compromises the formation of the more specialized motile cilia present in the embryonic node. Finally, misexpression of SP8 is sufficient to induce primary cilia formation in two unciliated cell types. Our findings demonstrate that SP5/8 are essential for cilia initiation in the embryo and sufficient to drive cilia formation in unciliated cells.
2025-06-25 | GSE273919 | GEO
Project description:Primary cilia play critical roles in sensory and signaling functions, and their dysregulation is associated with developmental abnormalities and multi-organ diseases. Despite their importance, the transcriptional regulation of primary cilia genes is unclear. Here, we employed transcriptome and mouse genetic tools to identify a master regulator of primary cilia genes. By comparing ciliated and non-ciliated cells in the early embryo using scRNA-seq and ChIP-seq, we uncovered that a wide spectrum of primary cilia genes are upregulated in ciliated cells and that SP5/8 within the SP/KLF family of transcription factors bind a core set of cilia genes. Loss- and gain-of-function assays in mouse embryos and embryonic stem cells demonstrate Sp5/8, are required for the initial formation of primary cilia in all embryonic cell types. Moreover, Sp5/8 loss compromises the formation of the more specialized motile cilia present in the embryonic node. Finally, misexpression of SP8 is sufficient to induce primary cilia formation in two unciliated cell types. Our findings demonstrate that SP5/8 are essential for cilia initiation in the embryo and sufficient to drive cilia formation in unciliated cells.
2025-06-25 | GSE273920 | GEO
Project description:Analysis of epithelial explants injected with the intracellular domain of Notch (ICD) to block the formation of multi-ciliate cells, either alone or along with FoxJ1. FoxJ1 misexpression leads to the induction fo ectopic cilia in Xenopus laevis epithelia. Results show which genes are affected by FoxJ1 during the induction of ectopic cilia. Ciliated cells that produce a leftward fluid flow have been proposed to mediate left-right patterning in many vertebrate embryos. These cilia combine features of primary sensory and motile cilia, but how such cilia are specified is unknown. We address this issue by analyzing the Xenopus and Zebrafish homologs of FoxJ1, a forkhead transcription factor necessary for ciliogenesis in multi-ciliate cells of the mouse. We show that the cilia that underlie left-right patterning on the Xenopus gastrocoel roof plate (GRP) and Zebrafish Kupffer’s vesicle (KV) are severely shortened or fail to form in FoxJ1 morphants. We also show that misexpressing XFoxJ1 is sufficient to induce ectopic GRP-like cilia formation in frog embryos. Microarray analysis indicates that XFoxJ1 induces the formation of cilia by upregulating the expression of motile cilia genes. These results indicate that FoxJ1 is a critical determinant in specifying cilia used in left-right patterning. Keywords: Cilia Induction
2008-09-15 | GSE12613 | GEO
Project description:Background: Whereas cilia damage and reduced cilia beat frequency have been implicated as causative of reduced mucociliary clearance in smokers, theoretically mucociliary clearance could also be affected by cilia length. Based on models of mucociliary clearance predicting cilia length must exceed the 6 -7 μm airway surface fluid depth to generate force in the mucus layer, we hypothesized cilia height may be decreased in airway epithelium of normal smokers compared to nonsmokers. Methodology/Principal Findings: Cilia length in normal nonsmokers and smokers was evaluated in aldehyde-fixed, paraffin-embedded endobronchial biopsies, and air-dried and hydrated samples brushed from human airway epithelium via fiberoptic bronchoscopy. In 28 endobronchial biopsies, healthy smoker cilia length was reduced 15% compared to nonsmokers (p<0.05). In 47 air-dried samples of airway epithelial cells, smoker cilia length was reduced 13% compared to nonsmokers (p<0.0001). Analysis of the length of individual, detached cilia in 17 samples, smoker cilia length was reduced 9% compared to nonsmokers (p<0.05). Finally, in 16 fully hydrated, unfixed samples, smoker cilia length was reduced 7% compared to nonsmokers (p<0.05). Conclusions/significance: Models predict that a reduction in cilia length would reduce mucociliary clearance, suggesting that smoking-associated shorter airway epithelial cilia plays a significant role in the pathogenesis of smoking-induced lung disease.
2012-12-13 | E-GEOD-16696 | biostudies-arrayexpress