Recombination at DNA replication fork barriers is not universal and is differentially regulated by Swi1.
DNA replication stress has been implicated in the etiology of genetic diseases, including cancers. It has been proposed that genomic sites that inhibit or slow DNA replication fork progression possess recombination hotspot activity and can form potential fragile sites. Here we used the fission yeast, Schizosaccharomyces pombe, to demonstrate that hotspot activity is not a universal feature of replication fork barriers (RFBs), and we propose that most sites within the genome that form RFBs do not have recombination hotspot activity under nonstressed conditions. We further demonstrate that Swi1, the TIMELESS homologue, differentially controls the recombination potential of RFBs, switching between being a suppressor and an activator of recombination in a site-specific fashion.
Pryce
David W
DW
North West Cancer Research Fund Institute, School of Biological Sciences, College of Natural Sciences, Bangor University, Bangor, Gwynedd, LL57 2UW, United Kingdom.
Ramayah
Soshila
S
Jaendling
Alessa
A
McFarlane
Ramsay J
RJ
D018797:Cell Cycle Proteins / Q000378:metabolism*; D004261:DNA Replication; D004268:DNA-Binding Proteins / Q000378:metabolism*; D008957:Models, Genetic; D011995:Recombination, Genetic / Q000235:genetics*; D012045:Regulatory Sequences, Nucleic Acid / Q000235:genetics; D012568:Schizosaccharomyces / Q000378:metabolism*; D029702:Schizosaccharomyces pombe Proteins / Q000378:metabolism*
D018797:Cell Cycle Proteins; D004268:DNA-Binding Proteins; D029702:Schizosaccharomyces pombe Proteins; C513096:swi1 protein, S pombe