fourfold increase in SCE events in Aldh2−/− mice (Fig. 1b, c, Extended Data Fig. 1a), suggesting that physiological acetaldehyde accumulation in blood cells is not sufficient to inactivate the homologous recombination repair factor BRCA216. Fancd2−/− mice do not show similar induction following exposure to ethanol; therefore, detoxification is the primary mechanism that prevents DNA damage by aldehydes and alcohol. Finally, the number of SCE events in Aldh2−/−Fancd2−/− mice is indistinguishable from that in Aldh2−/− mice, showing that homologous recombination repair occurs despite inactivation of FANCD2 (Fig. 1c, Extended Data Fig. 1b).
