Activity-DEPendent Transposition

Andrew G Newman; Paraskevi Bessa; Victor Tarabykin; Prim B Singh

doi:10.15252/embr.201643797

Activity-DEPendent Transposition

EMBO Rep. 2017 Mar;18(3):346-348. doi: 10.15252/embr.201643797. Epub 2017 Feb 20.

Authors

Andrew G Newman¹, Paraskevi Bessa¹, Victor Tarabykin^{1

2}, Prim B Singh^{1

3}

Affiliations

¹ Institute for Cell and Neurobiology, Charité Universitätsmedizin Berlin, Berlin, Germany.
² Lobachevsky State University of Nizhny Novgorod, Nizhny Novgorod, Russia.
³ Department of Natural Sciences and Psychology, Liverpool John Moores University, Liverpool, UK.

Abstract

The authors propose a novel mechanism, termed Activity‐DEPendent Transpositon (ADEPT), in which epigenetic drift and the preferential use of homologous‐directed repair allows transposable elements to hijack activity‐induced double‐strand breaks in aged neurons, contributing to neurodegenerative disease.

Publication types

Research Support, Non-U.S. Gov't

MeSH terms

Aging / genetics*
Animals
Brain / cytology
Brain / metabolism
DNA / genetics
DNA / metabolism
DNA Breaks, Double-Stranded
DNA End-Joining Repair
DNA Transposable Elements*
Epigenesis, Genetic*
Histones / genetics
Histones / metabolism
Humans
Mice
Nerve Net
Neuronal Plasticity / genetics*
Neurons / cytology
Neurons / metabolism*
Recombinational DNA Repair*

Substances

DNA Transposable Elements
Histones
DNA