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CAPN3 depletion causes continuously activated innate immune response in zebrafish

ABSTRACT: CAPN3 depletion causes continuously activated innate immune response in zebrafish

PROVIDER: PRJNA816527 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR18333106_1.fastq.gz	Fastqsanger.gz
	SRR18333106_2.fastq.gz	Fastqsanger.gz
	SRR18333107_1.fastq.gz	Fastqsanger.gz
	SRR18333107_2.fastq.gz	Fastqsanger.gz
	SRR18333108_1.fastq.gz	Fastqsanger.gz

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CAPN3 depletion causes continuously activated innate immune response in zebrafish

Project description:Capn3 is responsible for human disease LGMD2B, but the mechanism is largely unknown. We generated two capn3b-/- mutant zebrafish alleles and found that p53 is highly enriched in the hepatocyte nucleoli of capn3b knock-out fish. Although homozygous capn3b knock-out mutants are viable and fertile, they display shorter length and lateral curvature phenotype in adulthood, which is similar to the limb-girdle muscular dystrophy type 2A (LGMD2A) patients caused by capn3 mutation. Using RNA-seq analysis of adult liver, we identified differentially expressed genes in capn3b-/- mutants. Genes involved in innate immune response pathways were highly enriched in the mutants' livers. This study presents the connection between capn3 deficiency and immune defects and provides new insights into LGMD2B therapy.

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Project description:Circular RNAs (circRNAs) are widely expressed in eukaryotes. However, only a subset have been functionally characterized. We identify and validate a collection of circRNAs in Drosophila, and show that depletion of the brain-enriched circRNA Edis causes hyperactivation of antibacterial innate immunity both in cultured cells and in vivo. Notably, Edis depleted flies display heightened resistance to bacterial infection and enhanced pathogen clearance. Conversely, ectopic Edis expression blocks innate immunity signaling. In addition, inactivation of Edis in vivo leads to impaired locomotive activity and shortened lifespan. Remarkably, these phenotypes can be recapitulated with neuron-specific depletion of Edis, accompanied by defective neurodevelopment. Importantly, restoration of Edis expression suppresses both innate immunity and neurodevelopment phenotypes elicited by Edis depletion. We provide evidence that Edis encodes a functional protein that associates with and compromises the processing of the immune transcription factor Relish. Consistent with these observations, inactivation of Relish suppresses the innate immunity hyperactivation phenotype in the fly brain and rescues the neurodevelopment defects in Edis knockdown neurons. Thus, our study establishes the circRNA Edis as a key regulator of neurodevelopment and innate immunity.

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