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Fig. 1 Diverse ap2s1 alleles disrupt acoustically evoked habituation learning, responsiveness, and behavior selection bias (A) Diagram of AP2 complex, annotated with the zebrafish genes encoding each subunit. The heterotetrametric complex is composed of AP2α (ap2a1, green), AP2β (ap2b1, dark gray), AP2σ (ap2s1, red), and AP2μ (ap2m1a, ap2m1b, light gray). (B) Diagram of ap2s1 transcript and alleles, regions contributing to AP2 target binding indicated in orange with mutant disruptions indicated in red. (C‒H) Acoustic SLC habituation of wild type sibling (WT, blue), heterozygote sibling (Het, gray) and ap2s1 mutants (red), presented with 10 intense (23.8 dB) stimuli at 20s ISI, followed by 30 more identical stimuli at 1s ISI. Individual habituation scores were normalized to their baseline SLC response rate at 20s ISI (gray shading), and ap2s1 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 < 0.01, ∗∗∗p < 0.001, ∗∗∗∗p < 0.0001. Average SLC habituation scores across 300 identical stimuli at 1s ISI with hyperbolic fitted curves (F–H). (I‒K) Average responsiveness of individual larvae to 10 low intensity (−0.6 dB) acoustic stimuli presented at 20 s ISI, compared with two-tailed Mann-Whitney test with Bonferroni correction for multiple comparisons. (L‒N) Relative behavioral bias of individual larvae to 10 low intensity (−0.6 dB) acoustic stimuli presented at 20 s ISI, compared with two-tailed Mann-Whitney test with Bonferroni correction for multiple comparisons. Mutants (red) and heterozygotes (gray) were always compared to their corresponding wild type (blue) siblings, using ap2s1p172 (C, F, I, L), ap2s1hv1 (D, G, J, M), and ap2s1p199 (E, H, K, N) alleles. Data are represented as mean ± SEM in all panels and n indicates individual larvae. ∗p < 0.05, ∗∗p < 0.01, ∗∗∗p < 0.001, ∗∗∗∗p < 0.0001.