The presence of chromosome breaks and translocations indicates that aldehydes cause double-stranded breaks, which could be processed by non-homologous end-joining (NHEJ) repair17. Previous studies in cell lines and nematodes have indicated that, in the absence of the Fanconi anaemia pathway, engagement of double-stranded breaks by NHEJ leads to further genomic instability18,19. Therefore, we investigated whether NHEJ and Fanconi anaemia repair are redundant in resolving endogenous DNA damage in HSCs, and whether there is a role for NHEJ in maintaining resistance to acetaldehyde.
