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Microglia in developing retina transition through a disease-like functional state that does not require CSF1R signaling for survival

ABSTRACT: Microglia in developing retina transition through a disease-like functional state that does not require CSF1R signaling for survival

PROVIDER: PRJNA509754 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR8315010.fastq.gz	Fastqsanger.gz
	SRR8315011.fastq.gz	Fastqsanger.gz
	SRR8315012.fastq.gz	Fastqsanger.gz
	SRR8315013.fastq.gz	Fastqsanger.gz
	SRR8315004.fastq.gz	Fastqsanger.gz

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Microglia in developing retina transition through a disease-like functional state that does not require CSF1R signaling for survival

Project description:Microglia have important remodeling functions in development and disease. There is evidence for molecular diversity of microglia suggesting they may exist in distinct functional states to differentially impact CNS health and function. To better understand this in development, we profiled microglia of a discrete developing CNS region, the murine retina. We find that retinal microglia transition through unique transcriptional states and identify a population with peak density postnatally that resemble adult disease-associated microglia (DAM) and CD11c+ microglia of developing white matter, we term DAM-like. Developmental cell death is a major driver of the DAM-like phenotype, and TREM2 signaling is required for select DAM gene expression. Notably, DAM-like cells that highly express CD11c are not dependent on CSF1R signaling for survival, and TREM2 signaling is required for CSF1R independence in a subset of microglia. Thus, microglial phenotype in development is influenced by local developmental events and may share features with microglia in disease.

2019-06-10 | GSE123757 | GEO

Engineering an inhibitor resistant human CSF1R variant for microglia replacement [InVivo_RNA]

Project description:iPSC-derived hematopoietic progenitor cells expressing either the wildtype or G795A CSF1R variant were xenotransplanted into neonatal mice and subsequently aged for two months to compare in vivo gene expression differences between the two CSF1R genotypes.

2022-12-21 | GSE220214 | GEO

Engineering an inhibitor resistant human CSF1R variant for microglia replacement [InVitro_RNA]

Project description:iPSC-derived microglia expressing the wildtype, G795A, or G795C CSF1R variants were generated in vitro and treated with either DMSO or Plexxicon 5622 in order to compare the gene expression differences exising between genotypes at baseline or following CSF1R inhibtion.

2022-12-21 | GSE220213 | GEO

single-cell RNA-seq profile of adult microglia under acute Csf1r inhibition and early repopulation

Project description:Microglia are the resident myeloid cell in the central nervous system (CNS). Like other terminally differentiated myeloid cells, microglia rely on Csf1r signaling for survival and maintenance. Surprisingly, a small subset of microglia in the murine brain can survive without Csf1r signaling, as shown in Csf1r KO mice as well as in mice that have been treated with Csf1r inhibitor PLX5622. The nature of such Csf1r independent microglial population has not been fully characterized. Here we applied single-cell RNA-seq to examine the remaining microglia in C57/BL6J mice that were treated with PLX5622 diet (1200 mg/kg, 14 days), which results >90% microglial removal.

2019-12-01 | GSE133773 | GEO

Neuronal apoptosis drives remodeling states of microglia and shifts in survival pathway dependence [RNA-Seq]

Project description:Microglia serve critical remodeling roles that shape the developing nervous system, responding to the changing neural environment with phagocytosis or soluble factor secretion. Recent single-cell sequencing (scRNAseq) studies have revealed the context-dependent diversity in microglial properties and gene expression, but the cues promoting this diversity are not well defined. Here, we ask how interactions with apoptotic neurons shape microglial state, including lysosomal and lipid metabolism gene expression and dependence on Colony-stimulating factor 1 receptor (CSF1R) for survival. Using early postnatal mouse retina, a CNS region undergoing significant developmental remodeling, we performed scRNAseq on microglia from mice that are wild-type, lack neuronal apoptosis (Bax KO), or are treated with CSF1R inhibitor (PLX3397). We find that interactions with apoptotic neurons drives multiple microglial remodeling states, subsets of which are resistant to CSF1R inhibition. We find that TAM receptor Mer and complement receptor 3 are required for clearance of apoptotic neurons, but that Mer does not drive expression of remodeling genes. We show TAM receptor Axl is negligible for phagocytosis or remodeling gene expression but is consequential for microglial survival in the absence of CSF1R signaling. Thus, interactions with apoptotic neurons shift microglia towards distinct remodeling states and through Axl, alter microglial dependence on survival pathway, CSF1R.

2022-04-27 | GSE192601 | GEO

Neuronal apoptosis drives remodeling states of microglia and shifts in survival pathway dependence [scRNA-seq]

2022-04-27 | GSE192600 | GEO

Zebrafish control and csf1r mutant microglia transcriptomes

Project description:Purpose: Identify zebrafish control and csf1r-mutant microglia transcriptomes Methods: RNA sequencing was performed on FACS-sorted control microglia (3x), csf1ra-/- microglia (3x) and csf1ra-/-;b+/- microglia (3x). 10-20 million reads per sample were obtained. Reads were mapped to zebrafish genome GRC10. Results: We identified that csf1ra-/- or csf1ra-/-;b+/- microglia transcriptomes retain most of the microglia gene expression signature but mostly show changes in chemoklines expression.

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Zebrafish control and csf1r mutant microglia transcriptomes

Project description:Zebrafish control and csf1r mutant microglia transcriptomes

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single-cell RNA-seq profile of microglia under acute Csf1r inhibition and early repopulation in adult brain

2020-05-09 | GSE150169 | GEO

Differential CSF1R signaling enables widespread integration of genetically unmodified human microglia into the mouse brain

Project description:Microglia are long-lived myeloid cells in the central nervous system that are implicated in many neurological diseases. The differentiation of pluripotent stem cells provides an opportunity to develop in vitro human cellular models carrying disease gene mutations complementing existing animal models of disease. Microglia are particularly sensitive to their cellular environment and can adopt a variety of reactive states depending on different pathological conditions which may be difficult to mimic in vitro. Therefore, to best investigate human microglia in vivo, it would be helpful to generate mice whose endogenous microglia are exchanged with human cells without the need of genetic manipulation of donor cells which could alter microglia function. Colony stimulating factor 1 receptor (CSF1R) signaling is critical for microglial survival in mice, and humans with CSF1R mutations are born with fewer microglia. We made the surprising discovery that transplanted human pluripotent stem cell-derived microglia (hMG) survive pharmacological CSF1R inhibition unlike endogenous mouse microglia. Cellular assays confirmed that CSF1R signaling is necessary for human microglia survival and revealed differential CSF1R signaling with species-specific ligands. Moreover, receptor ligands and small molecule inhibitors acted in a competitive fashion. Based on these insights, we found that transient CSF1R inhibition after cell transplantation led to near-complete and wide-spread repopulation of hMGs into the mouse brain of immunodeficient mice with humanized CSF1 ligand. This approach allows the facile generation of mice whose brain microglia are replaced with genetically unmodified human cells.

2024-04-11 | GSE263618 | GEO

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