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Zebrafish are an emerging model organism to study the syndromic albinism disorder, Hermansky–Pudlak syndrome (HPS), due to visible pigment development at 24 hours postfertilization, and conserved melanogenesis mechanisms. We describe  crasher,  a novel HPS type 10 (HPS10) zebrafish model, with a mutation in AP‐3 complex subunit delta gene,  ap3d1 . Exon 14 of  ap3d1  is overexpressed in  crasher  mutants, while the expression of  ap3d1  as a whole is reduced . ap3d1  knockout in *AB zebrafish recapitulates the mutant  crasher  phenotype. We show  ap3d1  loss‐of‐function mutations cause significant expression changes in the melanogenesis genes, dopachrome tautomerase ( dct ) and tyrosinase‐related protein 1b ( tyrp1b ), but not tyrosinase ( tyr ). Last, Generally Applicable Gene‐set Enrichment (GAGE) analysis suggests autophagy pathway genes are upregulated together in  crasher.  Treatment with autophagy‐inhibitor, bafilomycin A1, significantly decreases melanophore number in  crasher,  suggesting  ap3d1  promotes melanophore survival by limiting excessive autophagy.  crasher  is a valuable model to explore the regulation of melanogenesis gene expression and pigmentation disease.

AP ‐3 complex subunit delta gene, ap3d1 , regulates melanogenesis and melanophore survival via autophagy in zebrafish ( Danio rerio )