Fig. 4: Synaptic connections between autophagy-deficient R7s and aberrant postsynaptic partners are functional based on activity-dependent GRASP.

a–c’ Activity-dependent GRASP between control R7s and Mi1s (a, a’), C2s (b, b’), and Mi4s (c, c’) show that wild-type R7s very rarely form synaptic connections, if any, with Mi1, C2, and Mi4 neurons. d–f’ Activity-dependent GRASP between atg6 mutant R7s and Mi1s (d, d’), C2s (e, e’), and Mi4s (f, f’) show widespread active synaptic connections between autophagy-deficient R7s and aberrant postsynaptic partners. g, i’, Activity-dependent GRASP between atg18 mutant R7s and Mi1s (g, g’), C2s (h, h’), and Mi4s (i, i’) show less frequent active synaptic connections compared with atg6 mutants. Note that Atg18 loss-of-function does not block autophagosome formation as effective as Atg6 loss-of-function (see Supplementary Fig. 1). Regions inside yellow rectangles are shown in close-up images as single greyscale GRASP channels. See Methods for Mi1, Mi4, and C2-specific LexA drivers and detailed Drosophila genotypes used to perform GRASP experiments. Repeated three times independently with similar results.