Ontology highlight
ABSTRACT:
PROVIDER: PRJNA459485 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR7119494.fastq.gz | Fastqsanger.gz | |||
| SRR7119495.fastq.gz | Fastqsanger.gz |
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Project description:CD47 is a key innate immune checkpoint that enables tumor cells to evade macrophage-mediated clearance. To systematically identify genetic regulators of CD47 surface expression, we performed FACS-based genome-wide CRISPR screens in three murine cancer cell lines, B16 (melanoma), MC38 (colon adenocarcinoma), and EMT6 (breast carcinoma). Comparative analysis of cells with high or low CD47 surface expression using DrugZ revealed CD47 itself as the top hit, validating the screens. Notably, DNAJC13 emerged as a consistent and robust regulator of CD47 expression across all three cell lines. Functional validation using DNAJC13-knockout cells confirmed a significant reduction in CD47 surface levels. Furthermore, in co-culture assays with macrophages, DNAJC13-deficient tumor cells exhibited increased susceptibility to phagocytosis, supporting a functional role for DNAJC13 in innate immune evasion. Finally, we verify that DNAJC13-knockout decrease tumor burden when treated with CD47 blockade. Overall, this study highlights a previously unrecognized regulator of CD47 and demonstrates the utility of high-throughput FACS-based CRISPR screening to uncover modulators of key immune checkpoint pathways.
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Project description:At least 70% of the human protein-coding genes possess more than one poly(A) site (PAS) and undergo a phenomenon known as alternative polyadenylation (APA), leading to distinct transcripts from a single gene. Previously, it has been demonstrated that shortening or lengthening of mRNA, resulting from the APA, could be observed in physiological and pathological conditions. Nevertheless, factors and cellular mechanisms responsible for the APA are largely unknown. CD47 protein localization was previously demonstrated to be regulated by APA. Here, we showed that core 3′ end processing factors regulate the different CD47 mRNA transcripts. This finding led us to develop an immunofluorescence staining method that simultaneously detects cell surface and intracellular CD47 protein and visualizes altered APA. Using this method, we detected the alterations of CD47 protein localization upon the depletion of the long 3′ untranslated region (UTR) mRNA isoform of CD47 or CFIm25. To systematically elucidate potential novel regulators of APA, we integrated an approach using immunofluorescence staining of cell surface and intracellular CD47 with genome-wide CRISPR screen coupled with pooled single guide RNA (sgRNA) libraries targeting human protein-coding genes. The functional genetic screens and systematic analysis of RNA-seq data revealed POLDIP2 as the potential novel regulator of APA that has global impact on APA regulation. These findings suggest that the study of novel identified APA regulators could lead to a deeper understanding of detailed molecular mechanisms governing APA under physiological and pathological conditions.
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Project description:CD47 is a ubiquitous cell surface receptor that limits cell clearance by phagocytes that express its counter-receptor signal-regulatory protein-α and directly regulates T cell immunity by interacting with its inhibitory ligand thrombospondin-1. Murine natural killer (NK) cells express higher levels of CD47 than other lymphocytes, but the role of CD47 in regulating NK cell homeostasis and immune function remains unclear. Cd47-/- mice exhibited depletion of NK precursors in bone marrow, but antisense Cd47 knockdown or gene disruption resulted in a dose dependent accumulation of immature and mature NK cells in spleen. Cd47-/- mice were impaired in controlling chronic Clone-13 lymphocytic choriomeningitis virus (LCMV) infection, which was associated with depletion of splenic NK cells and loss of effector cytokine and interferon response gene expression in Cd47-/- NK cells. These data identify CD47 as a cell-intrinsic and systemic regulator of NK cell homeostasis and NK cell responses to viral infection.
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Project description:A membrane protein SIRPα (CD172a) interacts with another membrane protein CD47 and thereby constitutes a cell–cell contact signal. To investigate the functional role of CD47-SIRPα signal in the brain, we analyzed the effect of genetic ablation of CD47-SIRPα signal on the gene expression profile in specific brain cells by the use of microarrays.
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Project description:A membrane protein SIRPα (CD172a) interacts with another membrane protein CD47 and thereby constitutes a cell–cell contact signal. To investigate the functional role of CD47-SIRPα signal in the brain, we analyzed the effect of genetic ablation of CD47-SIRPα signal on the gene expression profile in specific brain regions by the use of microarrays.
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Project description:Signaling through the thrombospondin-1 receptor CD47 broadly limits cell and tissue survival of stress, but the molecular mechanisms are incompletely understood. We now show that loss of CD47 permits sustained proliferation of primary murine endothelial cells and enables these cells to spontaneously reprogram to form multipotent embryoid bodies. c-Myc, Klf4, Oct4, and Sox2 expression is elevated in CD47-null endothelial cells, in several tissues of CD47- or thrombospondin-1-null mice, and in a human T cell line lacking CD47. CD47 knockdown acutely increases mRNA levels of c-Myc and other stem cell transcription factors in cells and in vivo, whereas CD47 ligation by thrombospondin-1 suppresses c-Myc expression. The inhibitory effects of increasing CD47 levels can be overcome by maintaining c-Myc expression and are absent in cells with dysregulated c-Myc. Thus, CD47 antagonists enable cell self-renewal and reprogramming by overcoming negative regulation of c-Myc and other stem cell transcription factors. To identify gene expression changes associated with CD47 null cells, we compared the gene expression profile of these cells with WT endothelial cell, CD47 null Embryoid bodies cells and an established Embryonic Stem cell line.
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