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Originally published as Genetics Published Articles Ahead of Print on February 4, 2007.

Genetics, Vol. 175, 1585-1595, April 2007, Copyright © 2007
doi:10.1534/genetics.106.067801

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Brc1-Mediated Rescue of Smc5/6 Deficiency: Requirement for Multiple Nucleases and a Novel Rad18 Function

Karen M. Lee*, Suzanne Nizza*, Thomas Hayes*, Kirstin L. Bass*, Anja Irmisch{dagger}, Johanne M. Murray{dagger} and Matthew J. O'Connell*,1

* Department of Oncological Sciences, Mount Sinai School of Medicine, New York, New York 10029 and {dagger} Genome Damage and Stability Centre, University of Sussex, Brighton BN1 9RQ, United Kingdom

1 Corresponding author: Department of Oncological Sciences, Mount Sinai School of Medicine, 1 Gustave L. Levy Place, Box 1130, New York, NY 10029.
E-mail: matthew.oconnell{at}mssm.edu

Smc5/6 is a structural maintenance of chromosomes complex, related to the cohesin and condensin complexes. Recent studies implicate Smc5/6 as being essential for homologous recombination. Each gene is essential, but hypomorphic alleles are defective in the repair of a diverse array of lesions. A particular allele of smc6 (smc6-74) is suppressed by overexpression of Brc1, a six-BRCT domain protein that is required for DNA repair during S-phase. This suppression requires the postreplication repair (PRR) protein Rhp18 and the structure-specific endonucleases Slx1/4 and Mus81/Eme1. However, we show here that the contribution of Rhp18 is via a novel pathway that is independent of PCNA ubiquitination and PRR. Moreover, we identify Exo1 as an additional nuclease required for Brc1-mediated suppression of smc6-74, independent of mismatch repair. Further, the Apn2 endonuclease is required for the viability of smc6 mutants without extrinsic DNA damage, although this is not due to a defect in base excision repair. Several nucleotide excision repair genes are similarly shown to ensure viability of smc6 mutants. The requirement for excision factors for the viability of smc6 mutants is consistent with an inability to respond to spontaneous lesions by Smc5/6-dependent recombination.




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Copyright © 2007 by the Genetics Society of America.