Base editing-derived models of human WDR34 and WDR60 disease alleles replicate retrograde intraflagellar transport (IFT) and hedgehog signaling defects.

Overexpression of wild-type WDR34 or WDR60 in the corresponding mutant cell lines partially rescued the delayed/impaired Golgi recovery after monensin treatment, with WDR60p.Ala911Val and WDR34p.Gly394Ser mutant clones displaying statistically significant recovery while clearly visible improvement of the golgi phenotype in WDR34p.Arg183Trp mutant cells did not quite reach statistical significance (Fig. 5J–M ).

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