Most germline mutations occur in males, but we still don’t know which stages of sperm development are most mutagenic. Using cell-sorting techniques and recent breakthroughs in long-read sequencing, we aim to map when, where, and how mutations arise during mammalian spermatogenesis. We aim to uncover the molecular mechanisms that allow germ cells to significantly reduce their mutation rate compared to somatic tissues.

Larger, long-lived species have evolved mechanisms to keep mutation rates low, presumably to counteract the harmful effects of mutations on cancer and ageing. Combining experimental and computational approaches, we are studying how cell lines from primates of different sizes and lifespans respond to DNA damage, aiming to identify the molecular processes that evolution has selected to develop healthier and longer-lived individuals.