Figure 6. Model of the role of OxPhos in Drosophila NSCs and tumour cells.

We propose a model, whereby highly proliferative Drosophila NSCs also rely on OxPhos for most aspects of their behaviour. In particular, the G₁/S transition depends on OxPhos activity and perturbation of this transition, either directly, or indirectly through OxPhos inhibition, results in delayed temporal patterning. This in turn prevents NSCs from terminating proliferation at the appropriate time, causing neurogenesis to persist into the adult. A similar dependence on OxPhos can be seen in brain tumours, where both proliferation and differentiation require mitochondrial activity, presumably through a similar mechanism to that found in normal NSCs.