Fig. 6: Loss of autophagy increases the number of synaptogenic filopodia through defective synaptic seeding factor degradation, leading to increased synapse formation throughout development.

a–c Quantification of filopodia numbers (a), synaptogenic filopodia numbers (b), and Brp puncta numbers (c) during synaptogenesis (P40–P90) per R7 axon terminal based on fixed data. n = 40 terminals per condition. d–f Markov State Model simulation based on data in (a) and live data at P + 60% (Fig. 5) for filopodia numbers (d), synaptogenic filopodia numbers (e), and Brp puncta numbers per R7 axon terminal (f). g The mechanistic model: accumulation of synaptic seeding factors stabilizes synaptogenic filopodia; autophagic degradation of synaptic seeding factors destabilizes filopodia. h Measured (solid bars) and simulated (striped bars) synaptogenic filopodia numbers at P + 60% (the simulated data are based on synaptic seeding factor availability, see Supplementary Fig. 6). n = 8 axon terminals from independent live-imaging sessions. i Representative images of synaptic seeding factors (Syd-1 and Liprin-α) localizing to synaptogenic filopodia. Repeated three times independently with similar results. j, k Quantifications of the number of Liprin-α (j) and Syd-1 (k) positive synaptogenic filopodia. n = 30 terminals per condition. Kruskal–Wallis and Dunn’s as post-hoc test; *p < 0.05, ***p < 0.001. Error bars denote mean ± SEM. Source data are provided as a Source Data file.