Germline stem cells (GSCs) from mammals to insects preferentially survive ionizing radiation but the underlying mechanisms are not well understood. Here we use the Drosophila testis to study the responses of GSCs to DNA damage in an intact tissue. We find that 75 Gy of ionizing radiation causes widespread DNA damage and rapidly reduces the GSC population by about half with GSCs lost from the niche via detachment rather than apoptosis. Remaining GSCs are functional, repopulating the niche. This series of events requires members of the canonical DNA damage response pathway, Chk2 and p53, to respond to double strand breaks induced by ionizing radiation. For survival, GSCs do not require the canonical nonhomologous end joining pathway members Ligase4 or Ku70 for DNA repair, but instead cell-autonomously require the homologous recombination factors Rad51 and Blm. In contrast with many other cells, which can use alternate repair mechanisms, our findings indicate that GSCs preferentially promote accurate DNA repair over error-prone repair, establishing the Drosophila testis as a model for studying stem cell DNA repair pathway choice in vivo.
Grey et al. (Fri,) studied this question.