Journal
DNA REPAIR
Volume 7, Issue 9, Pages 1426-1436Publisher
ELSEVIER SCIENCE BV
DOI: 10.1016/j.dnarep.2008.05.006
Keywords
Smc5-Smc6; gross chromosomal rearrangement; break-induced replication; checkpoints; translocations
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Funding
- National Human Genome Research Institute, National Institutes of Health
- Medical Research Council UK
- Medical Research Council [MC_U120074328] Funding Source: researchfish
- MRC [MC_U120074328] Funding Source: UKRI
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Translocations in chromosomes alter genetic information. Although the frequent translocations observed in many tumors suggest the altered genetic information by translocation could promote tumorigenesis, the mechanisms for how translocations are suppressed and produced are poorly understood. The smc6-9 mutation increased the translocation class gross chromosomal rearrangement (GCR). Translocations produced in the smc6-9 strain are unique because they are non-reciprocal and dependent on break-induced replication (BIR) and independent of non-homologous endjoining. The high incidence of translocations near repetitive sequences such as 6 sequences, ARS, tRNA genes, and telomeres in the smc6-9 strain indicates that Smc5-Smc6 suppresses translocations by reducing DNA damage at repetitive sequences. Synergistic enhancements of translocations in strains defective in DNA damage checkpoints by the smc6-9 mutation without affecting de novo telomere addition class GCR suggest that Smc5-Smc6 defines a new pathway to suppress GCR formation. Published by Elsevier B.V.
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