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Death by transposition - the enemy within?

John M Sedivy¹, Jill A Kreiling, Nicola Neretti

¹Department of Molecular Biology, Cell Biology and Biochemistry, Brown University, Providence, Rhode Island, USA.

Bioessays : News and Reviews in Molecular, Cellular and Developmental Biology

|October 17, 2013

Summary

This summary is machine-generated.

The reactivation of endogenous retrotransposable elements (RTEs) may be a key molecular aging process. Their activity could drive age-related tissue damage and disease.

Keywords:

aging anti-retroviral therapy cellular senescence retrotransposition

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Area of Science:

Molecular Biology
Genetics
Aging Research

Background:

Chromatin structure changes significantly during aging.
Cellular senescence is linked to reduced heterochromatinization and gene silencing.
Endogenous retrotransposable elements (RTEs) are normally silenced genomic sequences.

Purpose of the Study:

To propose and explore the hypothesis that derepression of RTEs is a molecular aging process.
To investigate the potential role of RTE activation in age-associated tissue degeneration and pathology.

Main Methods:

Literature review and hypothesis development.
Analysis of existing studies on chromatin dynamics, senescence, and RTEs.

Main Results:

RTEs comprise a significant portion of mammalian genomes and are typically silenced.
Aging is associated with chromatin rearrangements and decreased heterochromatinization.
Derepression of RTEs during aging is hypothesized to lead to transposition.

Conclusions:

The reactivation of endogenous retrotransposable elements is a novel hypothesis for a molecular aging process.
RTE activation may contribute to age-related tissue dysfunction and disease.
Further research into RTEs in aging is warranted.