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Mutagenesis Advance Access originally published online on January 12, 2009
Mutagenesis 2009 24(3):203-210; doi:10.1093/mutage/gen072
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© The Author 2009. Published by Oxford University Press on behalf of the UK Environmental Mutagen Society. All rights reserved. For permissions, please e-mail: journals.permissions@oxfordjournals.org.

Transcription-associated recombination in eukaryotes: link between transcription, replication and recombination

Ponnari Gottipati1 and Thomas Helleday1,2,*

1Gray Institute for Radiation Oncology and Biology, University of Oxford, Oxford OX3 7DQ, UK 2Department of Genetics Microbiology and Toxicology, Stockholm University, S-106 91 Stockholm, Sweden

Homologous recombination (HR) is an important DNA repair pathway and is essential for cellular survival. It plays a major role in repairing replication-associated lesions and is functionally connected to replication. Transcription is another cellular process, which has emerged to have a connection with HR. Transcription enhances HR, which is a ubiquitous phenomenon referred to as transcription-associated recombination (TAR). Recent evidence suggests that TAR plays a role in inducing genetic instability, for example in the THO mutants (Tho2, Hpr1, Mft1 and Thp2) in yeast or during the development of the immune system leading to genetic diversity in mammals. On the other hand, evidence also suggests that TAR may play a role in preventing genetic instability in many different ways, one of which is by rescuing replication during transcription. Hence, TAR is a double-edged sword and plays a role in both preventing and inducing genetic instability. In spite of the interesting nature of TAR, the mechanism behind TAR has remained elusive. Recent advances in the area, however, suggest a link between TAR and replication and show specific genetic requirements for TAR that differ from regular HR. In this review, we aim to present the available evidence for TAR in both lower and higher eukaryotes and discuss its possible mechanisms, with emphasis on its connection with replication.

* To whom correspondence should be addressed. Tel: +44 1865 617 324; Fax: +44 1865 857 127; Email: thomas.helleday{at}rob.ox.ac.uk

Received on September 9, 2008; revised on December 8, 2008; accepted on December 10, 2008.


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