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Mol. Cell. Biol. doi:10.1128/MCB.01335-06
Copyright (c) 2006, American Society for Microbiology and/or the Listed Authors/Institutions. All Rights Reserved.

Smc5/6 is required for repair at collapsed replication forks

Genome Damage and Stability Centre, University of Sussex, Brighton, BN1 9RQ, UK.; Department of Oncological Sciences, Mount Sinai School of Medicine, One Gustave L. Levy Place, Box 1130, New York, NY 10029, USA

^* To whom correspondence should be addressed. Email: j.m.murray{at}sussex.ac.uk.

	Abstract

In eukaryotes, three pairs of SMC proteins (Structural Maintenance of Chromosome) are found in conserved multi-subunit protein complexes required for chromosomal organisation. Cohesin, the Smc1/3 complex, mediates sister chromatid cohesion while two condensin complexes containing Smc2/4 facilitate chromosome condensation. Smc5/6 scaffolds an essential complex required for homologous recombination repair. We have examined the response of smc6 mutants to the inhibition of DNA replication. We define homologous recombination-dependent and -independent functions for Smc6 when replication is inhibited and provide evidence for a Rad60-independent function within S phase, in addition to a Rad60-dependent function post S phase. Both genetic and physical data show that, when forks collapse (i.e. are not stabilised by the Cds1^Chk2 checkpoint), Smc6 is required for the effective repair of resulting lesions but not for the recruitment of recombination proteins. We further demonstrate that when the Rad60-dependent post-S phase Smc6 function is compromised, the resulting recombination-dependent DNA intermediates that accumulate following release from replication arrest are not recognised by the G2/M checkpoint.

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