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Clec16a maintains the Definitive Hematopoietic Stem and Progenitor Cells via Mitophagy in Zebrafish

ABSTRACT: Since clec16a signaling is imperative for HSPCs production in zebrafish, to further determine the regulatory mechanism by which clec16a signaling regulates HSPCs. Bulk RNA sequencing analysis is performed to dissect the function and molecular mechanism between the control groups and the clec16a morphants groups.

ORGANISM(S): Danio rerio

PROVIDER: GSE281435 | GEO | 2026/01/06

REPOSITORIES: GEO

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Clec16a maintains the Definitive Hematopoietic Stem and Progenitor Cells via Mitophagy in Zebrafish

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

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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Nlrc3 signaling is required for hematopoietic stem cell emergence by activating Notch signaling in vertebrates

Project description:Purpose: Since Nlrc3 signaling is imperative for HSPCs production in zebrafish, to further determine the regulatory mechanism by which nlrc3 signaling regulates HSPCs. Bulk RNA sequencing analysis is performed to dissect the function and molecular mechanism between the control groups and the nlrc3 morphants groups. Methods: The GFP+ cells in Tg(fli1a:eGFP) zebrafish embryos at 28 hpf were sorted, which is the stage that EHT occurs in the VDA and the site of hemogenic endothelial cells onset. The mRNA profiles of these cells in wild-type (WT) and Nlrc3 knockdown were deep sequencing, in triplicate, using Illumina GAIIx. The sequence reads that passed quality filters were analyzed at the transcript isoform level with two methods: Burrows–Wheeler Aligner (BWA) followed by ANOVA (ANOVA) and TopHat followed by Cufflinks. qRT–PCR validation was performed using TaqMan and SYBR Green assays. Results: Using an optimized data analysis workflow, we mapped about 35 million sequence reads per sample and identified 4153 transcripts showing differential expression between the of WT and Nlrc3 morphants, with a fold change ≥1.5 and p value <0.05. Based on the results of RNA seq, some signaling pathways essential for the the Nlrc3 regulates the onset of HSPCs in vertebrate are dissected. Including Notch, WNT, NF-kB. Conclusions: Hemogenic endothelial cells mRNA profiles of WT groups and Nlrc3 knockdown groups were deep sequenced and anlysis. Based on the results of RNA seq, we performed experiments to validate the up and downstream pathway involved in the the Nlrc3 regulates the onset of HSCPs in vertebrate.

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