Figure EV3. Wrb disruption in hair cells causes a synaptopathic hearing impairment (related to Figs 3 and 7).

• A–A″
  ABR wave I amplitudes of Wrb ^+/+:Cre ^A and Wrb ^fl/fl control animals of groups I‐III are normal in transgenic animals lacking Cre expression.
• B
  ABR latencies of group I animals are increased in Wrb ^fl/fl:Cre ^A when compared to Wrb ^+/+:Cre ^A and Wrb ^fl/fl control animals.
• C
  Representative example frequency spectra of DPOAEs at 10.67 kHz measured from Wrb ^fl/fl:Cre ^A and Wrb ^+/+:Cre ^A mice to primary tones of 13.3 (70 dB) and 16 kHz (60 dB).
• D, E
  No statistically significant differences in (D) mean DPOAE amplitudes at increasing sound intensities in Wrb ^fl/fl:Cre ^A and Wrb ^+/+:Cre ^A (exemplary at 16 kHz) or (E) across the entire measured frequency range (at intensities of 70 dB (f1) and 60 dB (f2)) could be observed, indicating unaltered cochlear amplification and OHC function in the mutants.
• F
  IHC hair bundles appear normal in Wrb ^fl/fl:Cre ^A animals as assessed with fluorophore‐conjugated phalloidin stainings at P14. Scale bar: 5 μm.
• G
  Lack of ABR in > P63 Wrb ^fl/fl:Cre ^B mice across the entire frequency range. Upwards pointing arrowheads indicate thresholds exceeding the maximum speaker output of 90 dB.

Data information: All data are represented as mean ± SEM.