Evolutionarily Conserved Regulation of Immunity by the Splicing Factor RNP-6/PUF60
收藏干细胞与再生医学数据中心2022-02-20 更新2024-03-06 收录
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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.
提供机构：
Max Planck Institute for Biology of Ageing
创建时间：
2022-02-20
