Open Access
DMM Disease Models and Mechanisms
Premature aging in telomerase-deficient zebrafish
Anchelin Monique
1
,
Alcaraz-Pérez Francisca
1
,
Martínez Carlos M.
1
,
Bernabé-García Manuel
1
,
MULERO Victoriano
2
,
Cayuela María L.
1
1
University Hospital Virgen de la Arrixaca, Murcia, Spain;
|
2
University of Murcia, Murcia, SPAIN
|
Publication type: Journal Article
Publication date: 2013-01-01
Journal:
DMM Disease Models and Mechanisms
Quartile SCImago
Q1
Quartile WOS
Q2
Impact factor: 4.3
ISSN: 17548403, 17548411
PubMed ID:
23744274
General Biochemistry, Genetics and Molecular Biology
Medicine (miscellaneous)
Immunology and Microbiology (miscellaneous)
Neuroscience (miscellaneous)
Abstract
SUMMARY The study of telomere biology is crucial to the understanding of aging and cancer. In the pursuit of greater knowledge in the field of human telomere biology, the mouse has been used extensively as a model. However, there are fundamental differences between mouse and human cells. Therefore, additional models are required. In light of this, we have characterized telomerase-deficient zebrafish (Danio rerio) as the second vertebrate model for human telomerase-driven diseases. We found that telomerase-deficient zebrafish show p53-dependent premature aging and reduced lifespan in the first generation, as occurs in humans but not in mice, probably reflecting the similar telomere length in fish and humans. Among these aging symptoms, spinal curvature, liver and retina degeneration, and infertility were the most remarkable. Although the second-generation embryos died in early developmental stages, restoration of telomerase activity rescued telomere length and survival, indicating that telomerase dosage is crucial. Importantly, this model also reproduces the disease anticipation observed in humans with dyskeratosis congenita (DC). Thus, telomerase haploinsufficiency leads to anticipation phenomenon in longevity, which is related to telomere shortening and, specifically, with the proportion of short telomeres. Furthermore, p53 was induced by telomere attrition, leading to growth arrest and apoptosis. Importantly, genetic inhibition of p53 rescued the adverse effects of telomere loss, indicating that the molecular mechanisms induced by telomere shortening are conserved from fish to mammals. The partial rescue of telomere length and longevity by restoration of telomerase activity, together with the feasibility of the zebrafish for high-throughput chemical screening, both point to the usefulness of this model for the discovery of new drugs able to reactivate telomerase in individuals with DC.
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1 publication, 1.43%
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2
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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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Anchelin M. et al. Premature aging in telomerase-deficient zebrafish // DMM Disease Models and Mechanisms. 2013.
GOST all authors (up to 50)
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Anchelin M., Alcaraz-Pérez F., Martínez C. M., Bernabé-García M., MULERO V., Cayuela M. L. Premature aging in telomerase-deficient zebrafish // DMM Disease Models and Mechanisms. 2013.
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TY - JOUR
DO - 10.1242/dmm.011635
UR - https://doi.org/10.1242%2Fdmm.011635
TI - Premature aging in telomerase-deficient zebrafish
T2 - DMM Disease Models and Mechanisms
AU - Anchelin, Monique
AU - Alcaraz-Pérez, Francisca
AU - Martínez, Carlos M.
AU - Bernabé-García, Manuel
AU - MULERO, Victoriano
AU - Cayuela, María L.
PY - 2013
DA - 2013/01/01 00:00:00
PB - The Company of Biologists
PMID - 23744274
SN - 1754-8403
SN - 1754-8411
ER -
Cite this
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@article{2013_Anchelin,
author = {Monique Anchelin and Francisca Alcaraz-Pérez and Carlos M. Martínez and Manuel Bernabé-García and Victoriano MULERO and María L. Cayuela},
title = {Premature aging in telomerase-deficient zebrafish},
journal = {DMM Disease Models and Mechanisms},
year = {2013},
publisher = {The Company of Biologists},
month = {jan},
url = {https://doi.org/10.1242%2Fdmm.011635},
doi = {10.1242/dmm.011635}
}