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CLEC16A in astrocytes promotes mitophagy and limits pathology in a multiple sclerosis mouse model [bulk RNA-Seq]

ABSTRACT: CLEC16A in astrocytes promotes mitophagy and limits pathology in a multiple sclerosis mouse model [bulk RNA-Seq]

PROVIDER: PRJNA781235 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR16967300_1.fastq.gz	Fastqsanger.gz
	SRR16967300_2.fastq.gz	Fastqsanger.gz
	SRR16967301_1.fastq.gz	Fastqsanger.gz
	SRR16967301_2.fastq.gz	Fastqsanger.gz
	SRR16967302_1.fastq.gz	Fastqsanger.gz

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CLEC16A in astrocytes promotes mitophagy and limits pathology in a multiple sclerosis mouse model [Single Cell Dataset]

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CLEC16A in astrocytes promotes mitophagy and limits pathology in a multiple sclerosis mouse model [Single Cell Dataset]

Project description:Astrocytes promote neuroinflammation and neurodegeneration in multiple sclerosis (MS) through cell-intrinsic activities and their ability to recruit and activate other cell types. Here, in a genome-wide CRISPR-based forward genetic screen investigating regulators of astrocyte proinflammatory responses, we identified the C-type lectin domain-containing 16A gene (CLEC16A), linked to MS susceptibility, as a suppressor of nuclear factor-κB (NF-κB) signaling. Gene and small-molecule perturbation studies in mouse primary and human embryonic stem cell-derived astrocytes in combination with mitochodrial, metabolic and multiomic analyses established that CLEC16A promotes mitophagy, limiting mitochondrial dysfunction and the accumulation of mitochondrial products that activate NF-κB, the NLRP3 inflammasome and gasdermin D. Astrocyte-specific Clec16a inactivation increased NF-κB, NLRP3 and gasdermin D activation in vivo, worsening experimental autoimmune encephalomyelitis, a mouse model of MS. Moreover, we detected disrupted mitophagic capacity and gasdermin D activation in astrocytes in samples from individuals with MS. These findings identify CLEC16A as a suppressor of astrocyte pathological responses and a candidate therapeutic target in MS. Scheduled for publication in Nature Neuroscience DOI: 10.1038/s41593-025-01875-9

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