The many facets of homologous recombination at telomeres

Authors:

Clémence Claussin and Michael Chang

doi: 10.15698/mic2015.09.224
Volume 2, pp. 308 to 321, published 30/07/2015.

Affiliations:

European Research Institute for the Biology of Ageing, University of Groningen, University Medical Center Groningen, Groningen, The Netherlands.

Keywords: 

homologous recombination, telomeres, alternative lengthening of telomeres, telomerase-independent telomere maintenance, break-induced replication

Corresponding Author(s):

Michael Chang, European Research Institute for the Biology of Ageing, University of Groningen, University Medical Center Groningen, Antonius Deusinglaan 1; Groningen 9713 AV, The Netherlands m.chang@umcg.nl

Conflict of interest statement:

The authors declare that there are no conflicts of interest.

Please cite this article as:

Clémence Claussin and Michael Chang (2015). The many facets of homologous recombination at telomeres. Microbial Cell 2(9): 308-321

© 2015 Claussin and Chang. This is an open-access article released under the terms of the Creative Commons Attribution (CC BY) license, which allows the unrestricted use, distribution, and reproduction in any medium, provided the original author and source are acknowledged.

Abstract:

The ends of linear chromosomes are capped by nucleoprotein structures called telomeres. A dysfunctional telomere may resemble a DNA double-strand break (DSB), which is a severe form of DNA damage. The presence of one DSB is sufficient to drive cell cycle arrest and cell death. Therefore cells have evolved mechanisms to repair DSBs such as homologous recombination (HR). HR-mediated repair of telomeres can lead to genome instability, a hallmark of cancer cells, which is why such repair is normally inhibited. However, some HR-mediated processes are required for proper telomere function. The need for some recombination activities at telomeres but not others necessitates careful and complex regulation, defects in which can lead to catastrophic consequences. Furthermore, some cell types can maintain telomeres via telomerase-independent, recombination-mediated mechanisms. In humans, these mechanisms are called alternative lengthening of telomeres (ALT) and are used in a subset of human cancer cells. In this review, we summarize the different recombination activities occurring at telomeres and discuss how they are regulated. Much of the current knowledge is derived from work using yeast models, which is the focus of this review, but relevant studies in mammals are also included.