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Single-cell RNA sequencing of cortical samples in Fam69c knockout mice

ABSTRACT: Single-cell RNA sequencing of cortical samples in Fam69c knockout mice

PROVIDER: PRJNA839396 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR19271444.fastq.gz	Fastqsanger.gz
	SRR19271445.fastq.gz	Fastqsanger.gz
	SRR19271446.fastq.gz	Fastqsanger.gz
	SRR19271447.fastq.gz	Fastqsanger.gz
	SRR19271448.fastq.gz	Fastqsanger.gz

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Single-cell RNA sequencing of cortical samples in Fam69c knockout mice

Project description:Synapse loss and memory decline are the primary features of neurodegenerative dementia. However, molecular underpinnings that drive memory loss remain largely unknown. Here, we report that FAM69C is a novel kinase critically involved in neurodegenerative dementia. Biochemical analyses uncovered that FAM69C is a serine/threonine kinase. We generated the Fam69c knockout mice, and showed by single-cell RNA sequencing that FAM69C deficiency drives cell-type-specific transcriptional changes relevant to synapse dysfunction. Electrophysiological, morphological and behavioral experiments demonstrated impairments in synaptic plasticity, dendritic spine density and memory in Fam69c knockout mice, as well as stress-induced neuronal death. Phosphoproteomic characterizations revealed FAM69C substrates involved in synaptic structure and function. Finally, reduced levels of FAM69C were found in postmortem brains of AD. Our study demonstrates that FAM69C is a protective regulator of memory and suggests FAM69C as a potential therapeutic target for memory loss in neurodegenerative dementia.

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Project description:After central nervous system injury, a rapid neuroinflammatory response is induced. This response can be both beneficial and detrimental to neuronal survival in the first few days and increase the risk for neurodegeneration if it persists. Semaphorin4B (Sema4B), a transmembrane protein primarily expressed by cortical astrocytes, has been shown to play a role in neuronal cell death following injury. Our study shows that neuroinflammation is attenuated in Sema4B knockout mice and microglia/macrophage activation is reduced after cortical stab wound injury. In vitro, recombinant Sema4B enhances the activation of microglia following injury, suggesting astrocytic Sema4B functions as a ligand. Moreover, injury-induced activation of microglia is attenuated in the presence of Sema4B knockout astrocytes compared to heterozygous astrocytes. In vitro, experiments indicate Plexin-B2 is the Sema4B receptor on microglia. Consistent with this, microglia-specific Plexin-B2 knockout mice, similar to Sema4B knockout mice, also show a reduction in microglial activation after cortical injury. Finally, in Sema4B/Plexin-B2 double heterozygous mice, microglial activation is also reduced after injury, thus supporting the idea that both Sema4B and Plexin-B2 are part of the same signaling pathway. Taken together, we propose a model in which following injury, astrocytic Sema4B enhances the pro-inflammatory response of microglia/macrophages via Plexin-B2, leading to increased neuroinflammation.

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