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Mitochondrion-processed TERC regulates senescence without affecting telomerase activities

Authors :
Qian Zheng
Peipei Liu
Ge Gao
Jiapei Yuan
Pengfeng Wang
Jinliang Huang
Leiming Xie
Xinping Lu
Fan Di
Tanjun Tong
Jun Chen
Zhi Lu
Jisong Guan
Geng Wang
Source :
Protein & Cell, Vol 10, Iss 9, Pp 631-648 (2019)
Publication Year :
2019
Publisher :
Oxford University Press, 2019.

Abstract

Abstract Mitochondrial dysfunctions play major roles in ageing. How mitochondrial stresses invoke downstream responses and how specificity of the signaling is achieved, however, remains unclear. We have previously discovered that the RNA component of Telomerase TERC is imported into mitochondria, processed to a shorter form TERC-53, and then exported back to the cytosol. Cytosolic TERC-53 levels respond to mitochondrial functions, but have no direct effect on these functions, suggesting that cytosolic TERC-53 functions downstream of mitochondria as a signal of mitochondrial functions. Here, we show that cytosolic TERC-53 plays a regulatory role on cellular senescence and is involved in cognition decline in 10 months old mice, independent of its telomerase function. Manipulation of cytosolic TERC-53 levels affects cellular senescence and cognition decline in 10 months old mouse hippocampi without affecting telomerase activity, and most importantly, affects cellular senescence in terc −/− cells. These findings uncover a senescence-related regulatory pathway with a non-coding RNA as the signal in mammals.

Details

Language :
English
ISSN :
1674800X and 16748018
Volume :
10
Issue :
9
Database :
Directory of Open Access Journals
Journal :
Protein & Cell
Publication Type :
Academic Journal
Accession number :
edsdoj.3ef25a2d87674d1b9b077d07a90dc36d
Document Type :
article
Full Text :
https://doi.org/10.1007/s13238-019-0612-5