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. 2023 Jun 26;150(12):dev201552. doi: 10.1242/dev.201552

Fig. 5.

Fig. 5.

HBC-mediated neurogenesis following OE injury is attenuated by Notch1 cKO. (A-D) Relative to control (A,B), fewer HBC-derived PGP9.5+/tdTom+ OSNs (magenta in A and C; magenta outlines in B and D) constitute the morphologically regenerated OE at 28 dpi following HBC-specific Notch1 cKO (C,D). (E) Each circle represents an analyzed region, as represented in B and D (n=3 mice, 20 Notch1 WT regions and 20 Notch1 fl/fl regions). (F-I) Relative to control (F,G), OE composition of HBC-derived CK8+/apically localized IL33+/tdTom+ Sus cells (magenta in F and H; magenta outlines in G and I) at 28 dpi demonstrates no significant change following HBC-specific Notch1 cKO (H,I). (J) Each circle represents an analyzed region, as represented in G and I (n=3 mice, 18 Notch1 WT regions and 18 Notch1 fl/fl regions). Data are mean±s.e.m., unpaired t-test, ****P<0.0001 (E). Scale bar: 10 μm.