Insights & Perspectives
Death by transposition – the enemy within?
Article first published online: 15 OCT 2013
© 2013 The Authors. BioEssays published by WILEY Periodicals, Inc.
This is an open access article under the terms of the Creative Commons Attribution-NonCommercial License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited and is not used for commercial purposes.
Volume 35, Issue 12, pages 1035–1043, December 2013
How to Cite
Sedivy, J. M., Kreiling, J. A., Neretti, N., Cecco, M. D., Criscione, S. W., Hofmann, J. W., Zhao, X., Ito, T. and Peterson, A. L. (2013), Death by transposition – the enemy within?. Bioessays, 35: 1035–1043. doi: 10.1002/bies.201300097
- Issue published online: 18 NOV 2013
- Article first published online: 15 OCT 2013
- NIH/NIA. Grant Numbers: R37 AG016694, R01 AG035328
- Mentored Research Scientist Development Award
- NIH/NIA. Grant Number: K01 AG039410
- NIH/NCRR. Grant Number: P20 RR015578-10S1
- Mentored Quantitative Research Development Award
- NIH/NIA. Grant Numbers: K25 AG028753, K25 AG028753-03S1
- NIH/NIGMS Institutional Research Training. Grant Number: T32 GM007601
- NIH/NIA. Grant Number: F30 AG035592
- anti-retroviral therapy;
- cellular senescence;
Here we present and develop the hypothesis that the derepression of endogenous retrotransposable elements (RTEs) – “genomic parasites” – is an important and hitherto under-unexplored molecular aging process that can potentially occur in most tissues. We further envision that the activation and continued presence of retrotransposition contribute to age-associated tissue degeneration and pathology. Chromatin is a complex and dynamic structure that needs to be maintained in a functional state throughout our lifetime. Studies of diverse species have revealed that chromatin undergoes extensive rearrangements during aging. Cellular senescence, an important component of mammalian aging, has recently been associated with decreased heterochromatinization of normally silenced regions of the genome. These changes lead to the expression of RTEs, culminating in their transposition. RTEs are common in all kingdoms of life, and comprise close to 50% of mammalian genomes. They are tightly controlled, as their activity is highly destabilizing and mutagenic to their resident genomes.