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Jedi-1/MEGF12-mediated phagocytosis controls the pro-neurogenic properties of microglia in the ventricular-subventricular zone

ABSTRACT: Jedi-1/MEGF12-mediated phagocytosis controls the pro-neurogenic properties of microglia in the ventricular-subventricular zone

PROVIDER: PRJNA971985 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR24530310_1.fastq.gz	Fastqsanger.gz
	SRR24530310_2.fastq.gz	Fastqsanger.gz
	SRR24530311_1.fastq.gz	Fastqsanger.gz
	SRR24530311_2.fastq.gz	Fastqsanger.gz
	SRR24530312_1.fastq.gz	Fastqsanger.gz

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Jedi-1/MEGF12-mediated phagocytosis controls the pro-neurogenic properties of microglia in the ventricular-subventricular zone

Project description:Microglia are the primary phagocytes in the central nervous system and are responsible for clearing dead cells generated during development or disease. The phagocytic process shapes the phenotype of the microglia, which affects the local environment. A unique population of microglia reside in the ventricular-subventricular zone (V-SVZ) of neonatal mice, but how they influence this neurogenic niche is not well-understood. Here, we demonstrate that phagocytosis creates a pro-neurogenic microglial phenotype in the V-SVZ and that these microglia phagocytose apoptotic cells via the engulfment receptor Jedi-1. Deletion of Jedi-1 decreases apoptotic cell clearance, triggering the development of a neuroinflammatory phenotype, reminiscent of neurodegenerative and-age-associated microglia, that reduces neural precursor proliferation via elevated interleukin (IL)-1β signaling; inhibiton of IL-1 receptor rescues precursor proliferation in vivo. Together, these results reveal a critical role for Jedi-1 in connecting microglial phagocytic activity to a phenotype that promotes neurogenesis in the developing V-SVZ. We performed RNAseq on MACS-sorted microglia from V-SVZ and Cortex of WT and Jedi-1 knockout P7 mice.

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Single-cell gene expression of the subventricular zone (SVZ) neurogenic niche after partial reprogramming

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Jedi-1/MEGF12-mediated phagocytosis controls the pro-neurogenic properties of microglia in the ventricular-subventricular zone.

Project description:Microglia are the primary phagocytes in the central nervous system and are responsible for clearing dead cells generated during development or disease. The phagocytic process shapes the phenotype of the microglia, which affects the local environment. A unique population of microglia reside in the ventricular-subventricular zone (V-SVZ) of neonatal mice, but how they influence this neurogenic niche is not well-understood. Here, we demonstrate that phagocytosis creates a pro-neurogenic microglial phenotype in the V-SVZ and that these microglia phagocytose apoptotic cells via the engulfment receptor Jedi-1. Deletion of Jedi-1 decreases apoptotic cell clearance, triggering the development of a neuroinflammatory phenotype, reminiscent of neurodegenerative and-age-associated microglia, that reduces neural precursor proliferation via elevated interleukin (IL)-1β signaling; inhibition of IL-1 receptor rescues precursor proliferation in vivo. Together, these results reveal a critical role for Jedi-1 in connecting microglial phagocytic activity to a phenotype that promotes neurogenesis in the developing V-SVZ.

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Single cell analysis of the ventricular-subventricular zone reveals signatures of dorsal and ventral adult neurogenic lineages.

Project description:Single cell analysis of the ventricular-subventricular zone reveals signatures of dorsal and ventral adult neurogenic lineages.

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Single cell analysis of the ventricular-subventricular zone reveals signatures of dorsal and ventral adult neurogenic lineages. [single nucleus sequencing]

Project description:Purpose: While great progress has been made in understanding the differences in regional stem cell potential using viral and genetic lineage tracing strategies, the core molecular heterogeneity that underlies these regional differences is largely unknown. Methods: Here we present a single nucleus sequencing dataset of four microdissected regions of adult CD1 wild type mouse ventricular-subventricular zones (V-SVZ). Four samples (anterior-ventral, AV; anterior dorsal, AD; posterior ventral, PV; posterior dorsal, PD) were generated at the same time from the same mice, and each sample was run on its own lane of a 10x Chromium Single Cell Controller chip for single nucleus barcoding. Results: Here we present single nucleus and single whole cell sequencing datasets of microdissected adult mouse V-SVZ, and evidence for the existence of two broad subtypes of adult neural stem cells. By using spatially resolved microdissections in the single nucleus sequencing dataset as a reference, and mapping marker gene expression in the V-SVZ, we find that these two populations reside in largely non-overlapping domains in either the dorsal or ventral V-SVZ. Furthermore, we identified two subpopulations of newly born neurons that have gene expression consistent with dorsal or ventral origins. Finally, we identify genes expressed by both stem cells and the neurons they generate that specifically mark either the dorsal or ventral adult neurogenic lineage. These datasets, methods and findings will enable future study of region-specific regulation of adult neurogenesis.

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Project description:Single cell analysis of the ventricular-subventricular zone reveals signatures of dorsal and ventral adult neurogenic lineages. [single nucleus sequencing]

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Single cell analysis of the ventricular-subventricular zone reveals signatures of dorsal and ventral adult neurogenic lineages. [single whole-cell]

Project description:Single cell analysis of the ventricular-subventricular zone reveals signatures of dorsal and ventral adult neurogenic lineages. [single whole-cell]

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Interaction between subventricular zone microglia and neural stem cells impacts the neurogenic response in a mouse model of cortical ischemic stroke

Project description:After a stroke, the neurogenic response from the subventricular zone (SVZ) to repair the brain is limited. Microglia, as an integral part of the distinctive SVZ microenvironment, control neural stem / precursor cell (NSPC) behavior. Here, we show that discrete stroke-associated SVZ microglial clusters negatively impact the innate neurogenic response, and we propose a repository of relevant microglia–NSPC ligand–receptor pairs. After photothrombosis, a mouse model of ischemic stroke, the altered SVZ niche environment leads to immediate activation of microglia in the niche and an abnormal neurogenic response, with cell-cycle arrest of neural stem cells and neuroblast cell death. Pharmacological restoration of the niche environment increases the SVZ-derived neurogenic repair and microglial depletion increases the formation and survival of newborn neuroblasts in the SVZ. Therefore, we propose that altered cross-communication between microglial subclusters and NSPCs regulates the extent of the innate neurogenic repair response in the SVZ after stroke.

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Single-cell gene expression data from Ventricular-Subventricular Zone (V-SVZ) cells

Project description:Single-cell gene expression data from Ventricular-Subventricular Zone (V-SVZ) cells

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