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The association of Homologous recombination (HR) defects with numerous genetic diseases highlights the critical role of HR in maintaining genome stability. A key step in HR is the formation of Rad51 filaments that can perform homology search. We found that Rad51 filaments are subject to a tight regulation to avoid unproductive entities that can lead to cell death (Esta et al., PloS Genet, 2013). Mediator proteins, such as hBRCA2 in humans or yRad52 in the yeast Saccharomyces cerevisiae, drive Rad51 filament formation together with Rad51 paralogue proteins (like yRad55/yRad57) that prevent displacement of Rad51 filaments by several DNA helicases (hBLM, ySrs2…). ySrs2 is known to remove toxic Rad51 filaments, the nature of which is still not defined. In humans, most of these helicases are tumor suppressors, illustrating the importance of Rad51 filament regulation. Details of this regulation as well as the nature of toxic Rad51 filaments are far being understood. We are conducting genetics and biochemical experiments to describe precisely the nature of this regulation in the yeast Saccharomyces cerevisiae.
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