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Molecular regulatory mechanism and function of mitochondrial lncRNAs

Wednesday, September 24, 2014 — Poster Session IV

10:00 a.m. –12:00 p.m.

FAES Academic Center



* FARE Award Winner


  • JH Noh
  • M Gorospe


Mitochondrial dysfunction is associated with various aging-related diseases. Although the mitochondrial genome encodes proteins, a lot of mitochondrial proteins necessary for maintaining mitochondrial functions are imported from the nucleus. In addition, nuclear-encoded long-noncoding RNAs (lncRNAs) are required to maintain mitochondrial function. However, it is still unclear how RNAs are transported into mitochondria and what is the cellular role of the mitochondria-localized RNA species. From RNA-seq analysis, we identified nuclear-encoded lncRNAs localized in mitoplast. Among those lncRNAs, RPPH1 and RMRP were elevated in senescence fibroblasts compared to proliferating fibroblasts and were found to be the targets of RNA-binding proteins (RBPs) HuR and GRSF1. Importantly, GRSF1 silencing or HuR overexpression decreased oxygen consumption rate (OCR), highlighting key functions for these RBPs in mitochondrial respiration. Based on these data, we hypothesized the mitochondrial lncRNA import can be regulated by RBPs. To test this, we conducted experiments that (1) showed that RBPs regulate lncRNA import into mitochondria by observing lncRNA distribution in situ, (2) identified other protein or RNAs interacting with lncRNAs, and (3) discovered changing mitochondrial lncRNA distribution potently affected mitochondrial function. Through this work, we have gained critical knowledge of the mechanisms of through which regulatory RNAs are mobilized among cellular organelles.

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