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. 2022 Aug 5;221(9):e202112097. doi: 10.1083/jcb.202112097

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Figure 9. — Loss of KHC or PLP causes early Polo exposure and defective age dependent centriole segregation. (A) Polo::GFP is recruited early to the ganglion mother cell (GMC) inherited centrosome (yellow arrowhead) in isolated NBs expressing KHC or PoloRNAi. (B) Quantification of Polo asymmetry ∼18 min before metaphase (Control ASI: 0.63 ± 0.12, n = 29. PLPRNAi ASI: 0.33 ± 0.24 n = 28, KHCRNAi ASI: 0.37 ± 0.28 n = 28, ANOVA: P < 0.0001, Tukey pairwise comparison: Control vs PLPRNAi P < 0.0001, Control vs. KHCRNAi P = 0.0002). Error bars = SEM. (C) Example projections from whole mount brains showing that PLP localization is not perturbed in khc mutants (khc⁸/khc⁶³). (D) Quantification of PLP asymmetry in khc mutant NBs (Control ASI: −0.23 ± 0.03 n = 112 cells, eight brains. khc ASI: −0.024 ± 0.06 n = 123 cells, seven brains. Unpaired, two tailed, t test P = 0.7). Violins show ASI from all cells measured; points show averaged ASI per brain imaged. Errors bars = SD. (E) Isolated NBs expressing Cnb::GFP (cyan, arrowhead) to label the daughter centriole. In NBs also expressing KHC or PLP RNAi, the daughter centriole is more frequently segregated into the GMC. (F) Quantification of Cnb::GFP + centriole inheritance (% Cnb + centriole inherited by NB: Ctrl: 96%, PLPRNAi: 74%, KHCRNAi: 63%, 40 NBs were imaged per condition). Scale bars: 10 µm.