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Transcriptional profiles of microglia-like progeny cells derived from Cx3cr1 haplo-insufficient HSPCs and wild-tyoe HSPCs

ABSTRACT: Favoring the engraftment and maturation of the engineered HSPCs in the central nervous system could allow enhancing further the therapeutic potential of the transplantation of engineered HSPCs for treating neurometabolic diseases. We propose a gene addition strategy involving Cx3cr1, a microglia chemokine receptor regulating microglia ontogeny and function. Here we characterize the transcriptional profile of microglia-like cell generated by Cx3cr1 haplo-insufficient and WT HSPC

ORGANISM(S): Mus musculus

PROVIDER: GSE279132 | GEO | 2024/10/13

REPOSITORIES: GEO

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Transcriptional profiles of microglia-like progeny cells derived from Cx3cr1 haplo-insufficient HSPCs and wild-tyoe HSPCs

Project description:Transcriptional profiles of microglia-like progeny cells derived from Cx3cr1 haplo-insufficient HSPCs and wild-tyoe HSPCs

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Cx3cr1-deficient microglia exhibit a premature aging transcriptome

Project description:CX3CR1, one of the highest expressed genes in microglia in mice and humans, is implicated in numerous microglial functions. However, the molecular mechanisms underlying Cx3cr1 signaling are not well understood. Here, we analyzed transcriptomes of Cx3cr1-deficient microglia under varying conditions by RNA-Seq. In 2 mos mice, Cx3cr1 deletion resulted in the downregulation of a subset of immune-related genes, without substantial epigenetic changes in markers of active chromatin. Surprisingly, Cx3cr1-deficient microglia from young mice exhibited a transcriptome consistent with that of aged Cx3cr1-sufficient animals, suggesting a premature aging transcriptomic signature. Immunohistochemical analysis of microglia in young and aged mice revealed that loss of Cx3cr1 modulates microglial morphology in a compatible fashion. Our results suggest that CX3CR1 may regulate microglial function in part by modulating the expression levels of a subset of inflammatory genes during chronological aging, making Cx3cr1-deficient mice useful for studying aged microglia.

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Project description:This project defines the microglial gene expression profile in a transgenic mouse model of Alzheimer's, compared to non-transgenic age-matched controls, at a time when amyloid pathology and microgliosis are rampant. Microglia were sorted live from one hemisphere of cerebral cortex, using GFP expressed from Cx3cr1 locus (mice have one intact copy of Cx3cr1). RNA was isolated from sorted microglia using RNeasy mini. Two groups, PS2APP and non-transgenic, with 9 mice/group, aged 14-15 months. The "SAMPLE_ID" sample characteristic is a sample identifier internal to Genentech. The ID of this project in Genentech's ExpressionPlot database is PRJ0006715

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Cx3cr1-deficient microglia exhibit a premature aging transcriptome

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Cx3cr1-deficient microglia exhibit a premature aging transcriptome

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Mononuclear phagocytes in muscle after notexin injury in C57Bl/6, Cx3cr1-/-, Ccl2-/-,Cx3cr1-/-Ccl2-/- mice

Project description:Muscle injury triggers inflammation in which infiltrating mononuclear phagocytes are crucial for tissue regeneration. The interaction of the CCL2/CCR2 and CX3CL1/CX3CR1 chemokine axis that guides phagocyte infiltration is incompletely understood. Here, we show that CX3CR1 deficiency promotes muscle repair and rescues Ccl2-/- mice from impaired muscle regeneration as a result of altered macrophage function, not infiltration. Transcriptomic analysis of muscle mononuclear phagocytes reveals that Apolipoprotein E (ApoE) is up-regulated in mice with efficient regeneration. ApoE treatment enhances phagocytosis by mononuclear phagocytes in vitro, and restores phagocytic activity and muscle regeneration in Ccl2-/- mice. Because CX3CR1 deficiency may compensate for defective CCL2-dependant monocyte recruitment by modulating ApoE-dependent macrophage phagocytic activity, targeting CX3CR1 expressed by macrophages might be a powerful therapeutic approach to improve muscle regeneration.

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CX3CR1/Fractalkine receptor expression separates memory CD8+ T cells with distinct functional profiles (expression)

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Chromatin accessibility landscapes of CX3CR1+ effector , CX3CR1- Ly108- exhausted, or Ly108+ progenitor CD8 T cells during chronic viral infection.

Project description:During chronic viral infection, pathogen-specifc CD8+ T cells develop into three main phenotypically and functionally distinct subsets: TCF1hi progenitor, PD-1hi exhausted, and recently identied CX3CR1+ cytotoxic effector cells. Although genetic programs governing progenitor and exhausted subset formation have been well-studied, how CX3CR1+ effector CD8+ T cell differentiation is transcriptionally and epigentically regulated remains elusive. In this study, our single cell transcriptomics and epigenetic assays revealed that three subsets of virus-specific cells were governed by distinct gene regulatory networks (GRNs) and epigenetic landscapes. Computational analyses demonstrated a striking similarity between the CX3CR1+ subset and short-live effector cells (SLECs) from acute LCMV infection. Consistently, genetic deletion of T-bet (Tbx21) significantly diminished the formation and function of the CX3CR1+ subset. Importantly, we identify that the transcription factor (TF) BATF is required to maintain a permissive chromatin structure that allows differentiation transition from TCF1+ progenitor to CX3CR1+ effector cells. Intriguingly, haplodificiency of BATF in CD8+ T cells abolished CX3CR1+ effector subset formation. Lastly, we found that BATF directly bound to key genetic regions such as Tbx21 and modulated their enhancer accessibility to facilitate progenitor to CX3CR1+ effector cell transition. These mechanistic insights can be harnessed to overcome T cell exhaustion in treating chronic infections and cancer.

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