Mitochondrial Trafficking and Processing of Telomerase RNA TERC

Cell Rep. 2018 Sep 4;24(10):2589-2595. doi: 10.1016/j.celrep.2018.08.003.

Ying Cheng ¹, Peipei Liu ¹, Qian Zheng ¹, Ge Gao ¹, Jiapei Yuan ¹, Pengfeng Wang ², Jinliang Huang ¹, Leiming Xie ¹, Xinping Lu ¹, Tanjun Tong ³, Jun Chen ³, Zhi Lu ¹, Jisong Guan ¹, Geng Wang ⁴

Affiliations

1 MOE Key Laboratory of Bioinformatics, Cell Biology and Development Center, School of Life Sciences, Tsinghua University, Beijing 100084, China.
2 Peking University Research Center on Aging, Beijing 100191, China.
3 Peking University Research Center on Aging, Beijing 100191, China; Department of Biochemistry and Molecular Biology, Peking University Health Science Center, Beijing 100191, China.
4 MOE Key Laboratory of Bioinformatics, Cell Biology and Development Center, School of Life Sciences, Tsinghua University, Beijing 100084, China. Electronic address: wangeng@biomed.tsinghua.edu.cn.

PMID: 30184494 DOI: 10.1016/j.celrep.2018.08.003

Abstract

Mitochondrial dysfunctions play major roles in many diseases. However, how mitochondrial stresses are relayed to downstream responses remains unclear. Here we show that the RNA component of mammalian Telomerase TERC is imported into mitochondria, processed to a shorter form TERC-53, and then exported back to the cytosol. We found that the import is regulated by PNPASE, and the processing is controlled by mitochondrion-localized RNASET2. Cytosolic TERC-53 levels respond to changes in mitochondrial functions but have no direct effect on these functions. These findings uncover a mitochondrial RNA trafficking pathway and provide a potential mechanism for mitochondria to relay their functional states to Other cellular compartments.

Keywords

RNA; RNASET2; TERC; export; import; mitochondria; mitochondrial dysfunction; processing; retrograde signaling; telomerase.

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