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2015 ; 2
(9
): 308-321
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The many facets of homologous recombination at telomeres
#MMPMID28357308
Claussin C
; Chang M
Microb Cell
2015[Jul]; 2
(9
): 308-321
PMID28357308
show ga
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.
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