RT Journal Article
SR Electronic
T1 Smc6 And Top1 Prevent Aberrant Recombination At The Silent Mating-Type Locus HMR In Budding Yeast
JF bioRxiv
FD Cold Spring Harbor Laboratory Press
SP 134171
DO 10.1101/134171
A1 Martin Tran
A1 Camilla Sjogren
A1 Andreas Kegel
YR 2017
UL http://biorxiv.org/content/early/2017/05/04/134171.abstract
AB The structural maintenance of chromosomes 5/6 (Smc5/6) complex controls recombination in response to replicative stress, within the ribosomal DNA, and at telomeres. It has also been suggested to act in parallel with topoisomerase 1 (Top1) in the resolution of replication-induced superhelical stress under unperturbed conditions. In addition to this, human Smc5/6 was recently shown to suppress the expression of genes present on episomal DNA. The here presented study aimed to investigate the function of Smc5/6 at the transcriptionally silenced, heterochromatin-like loci HML and HMR in the budding yeast Saccharomyces cerevisiae. Using a silencing reporter assay and the temperature-sensitive smc6-56 mutant we found no evidence that Smc5/6 directly influences the maintenance or spreading of silenced domains. However, the results show that Smc6 associates with silent chromatin at HMR in a Sir2-dependent manner, and that Smc6 malfunction triggers aberrant recombination that leads to genomic rearrangement of HMR. This is also observed in top1Δ cells, and the results suggest that Smc5/6 and Top1 work in the same pathway. Taken together with results indicating that abnormal recombination in smc6-56 cells is suppressed by sir2Δ, this investigation indicates that Smc5/6 and Top1 act together to prevent aberrant recombination at the silenced mating-type loci HML and HMR. In the context of the already established functions of Smc5/6 and Top1, it suggests that unresolved replication-induced superhelical stress triggers recombination at silenced chromatin domains.