Fig. 8: Dh44 signalling from MP1 neurons tunes glial pyruvate routing.

Schematics illustrating the metabolic action of Dh44 signalling on cortex glia in the three conditions studied in the present work. Left: basal Dh44 release limits fatty acid synthesis in glia, through PKA activity, to levels that induce moderate LD formation, while glial support is dispensable for pyruvate supply to neuronal mitochondria. Middle: after flies learn of a danger-predictive cue, the enhanced metabolic activity of MB neuronal mitochondria is required to form threat-avoidance memory. Dh44 release by MP1 neurons is acutely enhanced. The resulting shutdown of ACC-mediated fatty acid synthesis makes glial pyruvate available for ALAT-mediated alanine conversion and export to neighbouring MB neurons. Right: when Dh44 signalling is shut down (genetic inhibition of Dh44 in MP1 neurons or Dh44-R1 in cortex glia), glial pyruvate massively flows into fatty acid synthesis, which results in extended LD production in glia and prevents metabolic support to neurons, thus preventing memory formation.