What mechanisms mediate developmental robustness in the face of inherent cellular variability, as well as diverse physical or metabolic constraints? Focused on a developing nervous system (that of the Drosophila larva), we have been asking: how can robust network function emerge from neuronal ensembles?

As developing networks become active, they undergo plastic tuning phases, termed ”critical periods”; ”critical” because disturbances during these developmental windows lead to lasting changes in function. To study the underlying mechanisms we have used the larval neuromuscular system as an experimental model. We find that transient embryonic experiences of different temperatures specify changes in synaptic terminal growth, neurotransmitter receptor composition and neuronal excitability. Moreover, the developmental timing of the critical period for muscles is distinct from that for neurons. We identified mitochondrial reactive oxygen species as key signals, and have preliminary insights on how such transient signals might be turned into lasting changes of gene expression and cellular properties.