Poly(ADP-ribose) polymerase (PARP-1) has a controlling role in homologous recombination

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Abstract
Cells with non‐functional poly(ADP‐ribose) polymerase (PARP‐1) show increased levels of sister chromatid exchange, suggesting a hyper recombination phenotype in these cells. To further investigate the involvement of PARP‐1 in homologous recombination (HR) we investigated how PARP‐1 affects nuclear HR sites (Rad51 foci) and HR repair of an endonuclease‐induced DNA double‐strand break (DSB). Several proteins involved in HR localise to Rad51 foci and HR‐deficient cells fail to form Rad51 foci in response to DNA damage. Here, we show that PARP‐1 mainly does not localise to Rad51 foci and that Rad51 foci form in PARP‐1–/– cells, also in response to hydroxyurea. Furthermore, we show that homology directed repair following induction of a site‐specific DSB is normal in PARP‐1‐inhibited cells. In contrast, inhibition or loss of PARP‐1 increases spontaneous Rad51 foci formation, confirming a hyper recombination phenotype in these cells. Our data suggest that PARP‐1 controls DNA damage recognised by HR and that it is not involved in executing HR as such.

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