PUBLICATION

Common dominant-negative spectrum of SLC45A2 mutations in OCA4 defined by endoplasmic reticulum retention

Authors
Urushibata, H., Shimizu, N., Yatsuka, H., Soga, Y., Inoue, M., Oki, R., Kubota, T., Takeda, A., Hanada, R., Ihara, K., Hanada, T.
ID
ZDB-PUB-260309-5
Date
2026
Source
Biochemical and Biophysical Research Communications   811: 153578 (Journal)
Registered Authors
Hanada, Reiko, Hanada, Toshikatsu
Keywords
Dominant-negative effect, Endoplasmic reticulum (ER), Oculocutaneous albinism type 4 (OCA4), SLC45A2, Zebrafish
MeSH Terms
none
PubMed
41797184 Full text @ Biochem. Biophys. Res. Commun.
Abstract
Oculocutaneous albinism type 4 (OCA4) is traditionally classified as an autosomal recessive disorder. Although the human Y70H variant has recently been suggested to exert a dominant-negative effect, it remains unknown whether this represents an isolated rarity or a manifestation of a broader pathogenic principle. Here, we identified a common dominant-negative SLC45A2 mutation spectrum based on its intracellular localization. Using a zebrafish model to systematically screen ten clinical variants, we identified four specific mutations, Y70H, D157 N, G188V, and L374F, which exerted potent dominant-negative effects in vivo. Subcellular localization analysis in B16 melanoma cells revealed that these mutant proteins exhibited significantly higher endoplasmic reticulum (ER) occupancy than the wild-type (WT) protein. Importantly, these variants act as "molecular traps" by physically sequestering WT SLC45A2 within the ER, thereby drastically reducing its delivery to TYRP1-positive melanosomes. Our findings demonstrate that dominant inheritance in OCA4 is driven by the spatial sequestration of functional proteins within the ER quality control machinery. This study establishes a new conceptual framework for the molecular diagnosis of OCA4 and provides a functional rationale for the use of pharmacological chaperones to rescue trapped transporters in membrane protein disorders.
Genes / Markers
Figures
Show all Figures
Expression
Phenotype
Mutations / Transgenics
Human Disease / Model
Sequence Targeting Reagents
Fish
Antibodies
Orthology
Engineered Foreign Genes
Mapping