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The evolutionarily conserved PRP4K-CHMP4B/vps32 splicing circuit regulates autophagy

ABSTRACT: The evolutionarily conserved PRP4K-CHMP4B/vps32 splicing circuit regulates autophagy

PROVIDER: PRJNA1242350 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR32868522_1.fastq.gz	Fastqsanger.gz
	SRR32868522_2.fastq.gz	Fastqsanger.gz
	SRR32868523_1.fastq.gz	Fastqsanger.gz
	SRR32868523_2.fastq.gz	Fastqsanger.gz

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The evolutionarily conserved PRP4K-CHMP4B/vps32 splicing circuit regulates autophagy

Project description:The pre-mRNA processing factor 4 kinase (PRP4K) is an essential gene in animal cells, making interrogation of its function challenging. Here, we report the first knockout model for PRP4K in the social amoeba Dictyostelium discoideum, revealing a new function in splicing events controlling autophagy. When prp4k knockout amoebae underwent multicellular development, we observed defects in differentiation linked to abnormal autophagy and aberrant secretion of stalk cell inducer c-di-GMP. Autophagosome-lysosome fusion was found to be impaired after PRP4K loss in both human cell lines and amoebae. Mechanistically, PRP4K loss results in mis-splicing and reduced expression of the ESCRT-III gene CHMP4B in human cells and its ortholog vps32 in Dictyostelium, and re-expression of CHMP4B or Vps32 cDNA (respectively) restored normal autophagosome-lysosome fusion in PRP4K-deficient cells. Thus, our work reveals a novel PRP4K-CHMP4B/vps32 splicing circuit regulating autophagy that is conserved over at least 600 million years of evolution.

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

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

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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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A transphyletic approach to analyzing evolutionarily conserved β-catenin modules

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