The AP2α subunit regulates acoustically evoked escape behavior (A) Diagram of ap2a1 transcript and disrupted splice donor site of ap2a1sa1907 (green). Core domain represented in orange and flexible appendage domain represented in blue. (B‒D) Acoustically evoked response modulation of wild types (blue, n = 36), heterozygotes (gray, n = 99) and ap2a1sa1907 mutants (green, n = 38). Average SLC habituation scores across 30 stimuli at 1s ISI (B), normalized to each individual’s baseline SLC response levels to 10 strong (23.8 dB) stimuli at 20s ISI. ap2a1 sa1907 mutants were compared to siblings with a 2-way repeated measures ANOVA (Genotype: p < 0.0001, Time: p < 0.0001, Individual: p < 0.0001), and significant pairwise comparisons (Dunnett’s test) vs. wild type are indicated, ∗∗∗∗p < 0.0001. Average responsiveness (C) and relative behavioral bias (D) of individuals to 10 weak (−6.7 dB) and 10 strong (23.8 dB) stimuli at 20 s ISI. ∗p < 0.05, ∗∗∗p < 0.001, ∗∗∗∗p < 0.0001, two-tailed Mann-Whitney test with Bonferroni correction for multiple comparisons. (E‒I) Average kinematic parameters of individual sibling (blue, n = 142) and ap2a1sa1907 mutant (green, n = 37) larvae in response to 40 strong (23.8 dB) acoustic stimuli, separated by SLC (left) and LLC (right) responses. Parameters measured were the initial response latency (E-F), maximum turning angle of the initial C-bend (G), initial C-bend duration (H), and maximum angular velocity of the initial C-bend (I). ∗∗∗p < 0.001, ∗∗∗∗p < 0.0001, two-tailed t-tests with Welch’s correction. Data are represented as mean ± SEM in all panels.
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