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Telomerase does not counteract telomere shortening but protects mitochondrial function under oxidative stress

Lookup NU author(s): Dr Saeed Ahmed, Dr Joao Passos, Matthew Birket, Dr Heiko Peters, Professor Mark Birch-Machin, Professor Thomas von Zglinicki, Dr Gabriele Saretzki

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Abstract

Telomerase is a ribonucleoprotein that counteracts telomere shortening and can immortalise human cells. There is also evidence for a telomere-independent survival function of telomerase. However, its mechanism is not understood. We show here that TERT, the catalytic subunit of human telomerase, protects human fibroblasts against oxidative stress. While TERT maintains telomere length under standard conditions, telomeres under increased stress shorten as fast as in cells without active telomerase. This is because TERT is reversibly excluded from the nucleus under stress in a dose- and tim-dependent manner. Extranuclear telomerase colocalises with mitochondria. In TERT-overexpressing cells, mtDNA is protected, mitochondrial membrane potential is increased and mitochondrial superoxide production and cell peroxide levels are decreased, all indicating improved mitochondrial function and diminished retrograde response. We propose protection of mitochondria under mild stress as a novel function of TERT.


Publication metadata

Author(s): Ahmed S, Passos JF, Birket MJ, Beckmann T, Brings S, Peters HH, Birch-Machin MA, von Zglinicki TW, Saretzki GC

Publication type: Article

Publication status: Published

Journal: Journal of Cell Science

Year: 2008

Volume: 121

Issue: 7

Pages: 1046-1053

ISSN (print): 0021-9533

ISSN (electronic): 1477-9137

Publisher: The Company of Biologists Ltd.

URL: http://dx.doi.org/10.1242/jcs.019372

DOI: 10.1242/jcs.019372

PubMed id: 18334557


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