The paper:
A. Sartori et al., “Human CtIP promotes DNA end resection,” Nature, 450:509–14, 2007. (Cited 135 times)
The finding:
Stephen Jackson and colleagues at the University of Cambridge, United Kingdom, showed that the protein CtIP, known to interact with tumor suppressor genes, could also help repair DNA double-strand breaks by homologous recombination, which uses the duplicate, unbroken chromosome as a template. A better understanding of the repair pathway can potentially lead to new targets for cancer, characterized by a flawed repair system.
The detail: The researchers knew that CtIP binds to another protein involved in homologous repair. When they would “zap [the cells] with a laser” to create double-strand breaks, says Jackson, they’d see CtIP—bound to GFP—light up at the damage site. This occurred only in S phase or G2, when the cell’s DNA was doubled. If zapped in G1, when the cell has only one copy of its ...
