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Gene therapy of Csf2ra-/- deficiency in long-term cultured fetal monocyte precursors restores bona fide alveolar macrophage development and function in mice

ABSTRACT: Gene therapy of Csf2ra-/- deficiency in long-term cultured fetal monocyte precursors restores bona fide alveolar macrophage development and function in mice

PROVIDER: PRJNA796565 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR17584871_1.fastq.gz	Fastqsanger.gz
	SRR17584871_2.fastq.gz	Fastqsanger.gz
	SRR17584872_1.fastq.gz	Fastqsanger.gz
	SRR17584872_2.fastq.gz	Fastqsanger.gz
	SRR17584873_1.fastq.gz	Fastqsanger.gz

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Gene therapy of Csf2ra-/- deficiency in long-term cultured fetal monocyte precursors restores bona fide alveolar macrophage development and function in mice

Project description:Tissue-resident macrophage-based immune therapies have been proposed for various diseases. However, generation of sufficient numbers that possess tissue-specific functions remains a major handicap. Here, we show that fetal liver monocytes cultured with GM-CSF (CSF2-cFLiMo) rapidly differentiate into a long-lived, homogeneous alveolar macrophage (AM)-like population in vitro. CSF2-cFLiMo remained the capacity to develop into bona fide AM upon transfer into Csf2ra-/- neonates and prevented development of alveolar proteinosis and accumulation of apoptotic cells for at least 1 year in vivo. CSF2-cFLiMo more efficiently engrafted empty AM niches in the lung and protected mice from severe pathology induced by respiratory viral infection, compared to transplantation of macrophages derived from bone marrow cells cultured with M-CSF (CSF1-cBMM) in the presence or absence of GM-CSF. Harnessing the potential of this approach for gene therapy, we restored a disrupted Csf2ra gene in FLiMo and demonstrated their capacity to develop into AM in vivo. Together, we provide a novel platform for generation of immature AM-like precursors amenable for genetic manipulation, which will be useful to dissect AM development and function and pulmonary transplantation therapy.

2022-01-15 | GSE193537 | GEO

CD74-NRG1 fusion as an bona fide oncogene

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Staphylococcus aureus bona fide sRNAs in the model strain HG003

Project description:Staphylococcus aureus bona fide sRNAs in the model strain HG003

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Staphylococcus aureus bona fide sRNAs in the model strain HG003

Project description:Accurate annotation of regulatory RNAs is a complex task but nevertheless essential as sRNA molecular and functional studies ensue from it. Several formerly considered small RNAs (sRNA) are now known to be parts of UTR transcripts. In light of experimental data, we review hundreds of Staphylococcus aureus putative regulatory RNAs. We pinpoint those that are likely acting in trans and are not expressed from the opposite strand of a coding gene. We conclude that HG003, a NCTC8325 derivative strain, has about 50 bona fide sRNAs, indicating that these RNAs are less numerous than commonly stated.

2018-03-07 | GSE104971 | GEO

Urine stem cells as a bona fide model to study cartilage associated disease

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Generation of Bona Fide Human Induced Trophoblast Stem Cells from Term Umbilical Cord

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Flt3 ligand expands bona fide innate lymphoid cell precursors in vivo.

Project description:A common helper-like innate lymphoid precursor (CHILP) restricted to the innate lymphoid cells (ILC) lineage has been recently characterized. While specific requirements of transcription factors for CHILPs development has been partially described, their ability to sense cytokines and react to peripheral inflammation remains unaddressed. Here, we found that systemic increase in Flt3L levels correlated with the expansion of Lineage (Lin)negα4β7+ precursors in the adult murine bone marrow. Expanded Linnegα4β7+ precursors were bona fide CHILPs as seen by their ability to differentiate into all helper ILCs subsets but cNK in vivo. Interestingly, Flt3L-expanded CHILPs transferred into lymphopenic mice preferentially reconstituted the small intestine. While we did not observe changes in serum Flt3L during DSS-induced colitis in mice or plasma from inflammatory bowel disease (IBD) patients, elevated Flt3L levels were detected in acute malaria patients. Interestingly, while CHILP numbers were stable during the course of DSS-induced colitis, they expanded following increased serum Flt3L levels in malaria-infected mice, hence suggesting a role of the Flt3L-ILC axis in malaria. Collectively, our results indicate that Flt3L expands CHILPs in the bone marrow, which might be associated with specific inflammatory conditions.

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BioE3 enables the identification of bona fide targets of E3 ligases

Project description:The post-translational modification of proteins by ubiquitination is a highly regulated process that involves a dynamic, three-step enzymatic cascade, where more than 600 E3 ligases play a critical role in recognizing specific substrates for modification. Separating bona fide targets of E3s from E3-interacting proteins remains a major challenge in the field. In this study, we present BioE3, a novel approach for identifying substrates of ubiquitin-like (UbL) E3 ligases of interest. Using BirA-E3 ligase fusion proteins and bioUbLs, the method facilitates site-specific biotinylation of UbL-modified substrates for proteomic identification. We demonstrate that the BioE3 system can identify both known and novel targets of two RING-type ubiquitin E3 ligases: RNF4, known to be involved in DNA damage response and the regulation of PML nuclear bodies, and MIB1, implicated in endocytosis, autophagy, and centrosomal protein homeostasis. We further show the versatility of BioE3 by identifying targets of an organelle-specific E3 (MARCH5) and a relatively uncharacterized E3 (RNF214). Furthermore, we show that BioE3 works with HECT-type E3 ligases and identify novel targets of NEDD4 involved in vesicular trafficking. BioE3 is a powerful tool that enables identification of bona fide substrates of UbL E3 ligases and how they change with chemical perturbations, which may be useful for the emerging applications in targeted protein degradation (TPD). BioE3 may also be applicable for UbLs beyond Ub and SUMO, as well as other E3 ligase classes. The resulting knowledge can shed light on the regulation of cellular processes by the complex UbL network, advancing our understanding of fundamental biological mechanisms.

2024-01-26 | PXD041685 | Pride

Transcriptomic analysis unveils bona fide molecular signatures of microglia under conditions of homeostasis and viral encephalitis

Project description:Microglia provide a front-line defense against neuroinvasive viral infection, however, determination of their bona fide transcriptional profiles under conditions of health and disease is challenging. Here, we used a combination of experimental tools to delineate the overall transcriptional landscape of microglia during viral infection. By exploiting the ribosomal tagging approach, we developed the concept of enrichment of relevant marker genes by comparing immunoprecipitated RNA with total RNA. Enriched transcripts corresponding to genes expressed in target cells were instrumental in defining bona fide signatures of microglia. With this approach, we generated a comprehensive and accurate transcriptome of microglia at the in situ environment under conditions of health and virus infection. These unified microglial signatures may serve as a benchmark to retrospectively assess ex vivo artefacts from available atlases. Leveraging the microglial translatome, we found enrichment of genes implicated in T-cell activation and cytokine production during the course of VSV infection. These data linked microglia with T-cell re-stimulation and further underscored that microglia shape anti-viral T-cell responses in the brain. Collectively, this study faithfully defines the transcriptional landscape of microglia in steady state and during viral encephalitis and highlights cellular interactions between microglia and T cells that contribute to the control of virus dissemination.

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