Open Access
Nature Communications, volume 11, issue 1, publication number 1168
The mTOR pathway is necessary for survival of mice with short telomeres
Ferrara Romeo Iole
1
,
Martinez Paula
1
,
Saraswati Sarita
1
,
Whittemore Kurt
1
,
Graña-Castro Osvaldo
2
,
Thelma Poluha Lydia
1
,
Serrano Rosa
1
,
Hernández Encinas Elena
3
,
Blanco-Aparicio Carmen
3
,
Maria Flores Juana
4
,
Blasco María A
1
1
Telomeres and Telomerase Group, Molecular Oncology Program, Spanish National Cancer Centre (CNIO), Madrid, Spain
|
2
Bioinformatics Unit, Structural Biology and Biocomputing Program, Spanish National Cancer Centre (CNIO), Madrid, Spain
|
3
Experimental Therapeutics Program, Spanish National Cancer Centre (CNIO), Madrid, Spain
|
4
Animal Surgery and Medicine Department, Faculty of Veterinary Science, Complutense University of Madrid, Madrid, Spain
|
Publication type: Journal Article
Publication date: 2020-03-03
Journal:
Nature Communications
Quartile SCImago
Q1
Quartile WOS
Q1
Impact factor: 16.6
ISSN: 20411723
PubMed ID:
32127537
General Chemistry
General Biochemistry, Genetics and Molecular Biology
General Physics and Astronomy
Abstract
Telomerase deficiency leads to age-related diseases and shorter lifespans. Inhibition of the mechanistic target of rapamycin (mTOR) delays aging and age-related pathologies. Here, we show that telomerase deficient mice with short telomeres (G2- Terc −/− ) have an hyper-activated mTOR pathway with increased levels of phosphorylated ribosomal S6 protein in liver, skeletal muscle and heart, a target of mTORC1. Transcriptional profiling confirms mTOR activation in G2- Terc −/− livers. Treatment of G2- Terc −/− mice with rapamycin, an inhibitor of mTORC1, decreases survival, in contrast to lifespan extension in wild-type controls. Deletion of mTORC1 downstream S6 kinase 1 in G3- Terc −/− mice also decreases longevity, in contrast to lifespan extension in single S6K1 −/− female mice. These findings demonstrate that mTOR is important for survival in the context of short telomeres, and that its inhibition is deleterious in this setting. These results are of clinical interest in the case of human syndromes characterized by critically short telomeres. Telomerase deficiency leads to age-related diseases and shortened lifespan, while inhibition of the mTOR pathway delays aging. Here, the authors show that inhibition of mTORC1 signaling shortens the lifespan of telomerase deficient mice.
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- We do not take into account publications that without a DOI.
- Statistics recalculated only for publications connected to researchers, organizations and labs registered on the platform.
- Statistics recalculated weekly.
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Ferrara Romeo I. et al. The mTOR pathway is necessary for survival of mice with short telomeres // Nature Communications. 2020. Vol. 11. No. 1. 1168
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Ferrara Romeo I., Martinez P., Saraswati S., Whittemore K., Graña-Castro O., Thelma Poluha L., Serrano R., Hernández Encinas E., Blanco-Aparicio C., Maria Flores J., Blasco M. A. The mTOR pathway is necessary for survival of mice with short telomeres // Nature Communications. 2020. Vol. 11. No. 1. 1168
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TY - JOUR
DO - 10.1038/s41467-020-14962-1
UR - https://doi.org/10.1038%2Fs41467-020-14962-1
TI - The mTOR pathway is necessary for survival of mice with short telomeres
T2 - Nature Communications
AU - Ferrara Romeo, Iole
AU - Martinez, Paula
AU - Saraswati, Sarita
AU - Whittemore, Kurt
AU - Graña-Castro, Osvaldo
AU - Thelma Poluha, Lydia
AU - Serrano, Rosa
AU - Hernández Encinas, Elena
AU - Blanco-Aparicio, Carmen
AU - Maria Flores, Juana
AU - Blasco, María A
PY - 2020
DA - 2020/03/03 00:00:00
PB - Springer Nature
IS - 1
VL - 11
PMID - 32127537
SN - 2041-1723
ER -
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@article{2020_Ferrara Romeo,
author = {Iole Ferrara Romeo and Paula Martinez and Sarita Saraswati and Kurt Whittemore and Osvaldo Graña-Castro and Lydia Thelma Poluha and Rosa Serrano and Elena Hernández Encinas and Carmen Blanco-Aparicio and Juana Maria Flores and María A Blasco},
title = {The mTOR pathway is necessary for survival of mice with short telomeres},
journal = {Nature Communications},
year = {2020},
volume = {11},
publisher = {Springer Nature},
month = {mar},
url = {https://doi.org/10.1038%2Fs41467-020-14962-1},
number = {1},
doi = {10.1038/s41467-020-14962-1}
}