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Evolutionarily Conserved Regulation of Immunity by the Splicing Factor RNP-6/PUF60

ABSTRACT: Evolutionarily Conserved Regulation of Immunity by the Splicing Factor RNP-6/PUF60

PROVIDER: PRJNA592073 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR10544927_1.fastq.gz	Fastqsanger.gz
	SRR10544927_2.fastq.gz	Fastqsanger.gz
	SRR10544928_1.fastq.gz	Fastqsanger.gz
	SRR10544928_2.fastq.gz	Fastqsanger.gz
	SRR10544929_1.fastq.gz	Fastqsanger.gz

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Evolutionarily Conserved Regulation of Immunity by the Splicing Factor RNP-6/PUF60

Project description:Splicing is a vital cellular process that modulates important aspects of animal physiology, including metabolism and lifespan. From a cold stress screen, we identified a novel mutant of the splicing factor RNP-6/PUF60, which evokes resistance to various abiotic stresses, yet is highly sensitive to pathogenic bacterial challenge. Molecular and genetic experiments reveal that RNP-6 suppresses immunity, but promotes animal longevity, suggesting a tradeoff between these processes. Pathogen exposure affects gene expression and splicing in a rnp-6 dependent manner. Another longevity promoting splicing factor, SFA-1, similarly exerts an immuno-suppressive effect, working downstream or parallel to RNP-6. Genetic epistasis and biochemical experiments reveal that RNP-6 acts through PMK-1 MAPK signaling to modulate immunity. The mammalian homolog, PUF60, also displays anti-inflammatory properties, and its levels swiftly decrease after bacterial infection in mammalian cells. Our findings demonstrate an evolutionarily conserved modulation of immunity by specific components of the splicing machinery.

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An evolutionarily conserved function of the pre-mRNA splicing regulator TNPO3 for T cell development

Project description:All vertebrates possess lymphocytes, enabling the functional interrogation of this evolutionarily conserved organizing principle of adaptive immunity in non-mammalian species. A forward genetic screen in zebrafish indicated that a mutation of tnpo3, encoding a regulator of alternative splicing of pre-mRNAs, specifically impaired intrathymic T cell development. In mouse T cells, Tnpo3 deficiency predominantly disrupted the splicing of genes encoding RNA-binding motifs, and it specifically blocked the splicing of Va11, associated with reduced numbers of peripheral T cells and the complete loss of iNKT cells. Our results reveal an evolutionarily conserved function of a pre-mRNA processing factor for T cell development, uncovering a previously unappreciated checkpoint during the formation of mature mRNAs of the Tcra gene.

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Evolutionarily conserved regulation of immunity by the splicing factor RNP-6/PUF60.

Project description:Splicing is a vital cellular process that modulates important aspects of animal physiology, yet roles in regulating innate immunity are relatively unexplored. From genetic screens in C. elegans, we identified splicing factor RNP-6/PUF60 whose activity suppresses immunity, but promotes longevity, suggesting a tradeoff between these processes. Bacterial pathogen exposure affects gene expression and splicing in a rnp-6 dependent manner, and rnp-6 gain and loss-of-function activities reveal an active role in immune regulation. Another longevity promoting splicing factor, SFA-1, similarly exerts an immuno-suppressive effect, working downstream or parallel to RNP-6. RNP-6 acts through TIR-1/PMK-1/MAPK signaling to modulate immunity. The mammalian homolog, PUF60, also displays anti-inflammatory properties, and its levels swiftly decrease after bacterial infection in mammalian cells, implying a role in the host response. Altogether our findings demonstrate an evolutionarily conserved modulation of immunity by specific components of the splicing machinery.

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