Hsp90 picks PIKKs via R2TP and Tel2

Phosphatidylinositol-3 kinase-like kinases (PIKKs) are dependent on Hsp90 for their activation via the R2TP complex and Tel2. In this issue of Structure, Pal and colleagues present the molecular mechanism by which PIKKs are recruited to Hsp90

DNA resection in eukaryotes: deciding how to fix the break

DNA double-strand breaks are repaired by different mechanisms, including homologous recombination and nonhomologous end-joining. DNA-end resection, the first step in recombination, is a key step that contributes to the choice of DSB repair. Resection, an evolutionarily conserved process that generates single-stranded DNA, is linked to checkpoint activation and is critical for survival. Failure to regulate and execute this process results in defective recombination and can contribute to human disease. Here, I review recent findings on the mechanisms of resection in eukaryotes, from yeast to vertebrates, provide insights into the regulatory strategies that control it, and highlight the consequences of both its impairment and its deregulation