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Dual loss of human POLQ and LIG4 abolishes random integration.

Abstract：

:Homologous recombination-mediated gene targeting has greatly contributed to genetic analysis in a wide range of species, but is highly inefficient in human cells because of overwhelmingly frequent random integration events, whose molecular mechanism remains elusive. Here we show that DNA polymerase θ, despite its minor role in chromosomal DNA repair, substantially contributes to random integration, and that cells lacking both DNA polymerase θ and DNA ligase IV, which is essential for non-homologous end joining (NHEJ), exhibit 100% efficiency of spontaneous gene targeting by virtue of undetectable levels of random integration. Thus, DNA polymerase θ-mediated end joining is the sole homology-independent repair route in the absence of NHEJ and, intriguingly, their combined absence reveals rare Alu-Alu recombination events utilizing a stretch of homology. Our findings provide new insights into the mechanics of foreign DNA integration and the role of DNA polymerase θ in human genome maintenance.

journal_name

Nat Commun

journal_title

Nature communications

authors

Saito S,Maeda R,Adachi N

doi

10.1038/ncomms16112

subject

Has Abstract

pub_date

2017-07-11 00:00:00

pages

16112

issn

2041-1723

pii

ncomms16112

journal_volume

8

pub_type

杂志文章

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