PUBLICATION

Cryo-EM structure of the BLOC-3 complex provides insights into the pathogenesis of Hermansky-Pudlak syndrome

Authors
Yong, X., Jia, G., Yang, Q., Zhou, C., Zhang, S., Deng, H., Billadeau, D.D., Su, Z., Jia, D.
ID
ZDB-PUB-250327-18
Date
2025
Source
Nature communications   16: 29672967 (Journal)
Registered Authors
Keywords
none
MeSH Terms
  • Protein Domains
  • Animals
  • Protein Binding
  • Guanine Nucleotide Exchange Factors
  • Models, Molecular
  • Melanosomes/metabolism
  • Melanosomes/ultrastructure
  • Carrier Proteins
  • Membrane Proteins/chemistry
  • Membrane Proteins/genetics
  • Membrane Proteins/metabolism
  • Hermanski-Pudlak Syndrome*/genetics
  • Hermanski-Pudlak Syndrome*/metabolism
  • Hermanski-Pudlak Syndrome*/pathology
  • rab GTP-Binding Proteins*/genetics
  • rab GTP-Binding Proteins*/metabolism
  • Humans
  • Mutation
  • GTP Phosphohydrolases/chemistry
  • GTP Phosphohydrolases/genetics
  • GTP Phosphohydrolases/metabolism
  • Cryoelectron Microscopy*
  • HEK293 Cells
  • Zebrafish*
PubMed
40140412 Full text @ Nat. Commun.
Abstract
Biogenesis of lysosome-related organelle complex-3 (BLOC-3) is pivotal in vesicle trafficking and has been linked to Hermansky-Pudlak syndrome (HPS). Despite its importance, the structure and molecular function of BLOC-3 remains elusive. Here, we report the Cryo-EM structure of human BLOC-3 at 3.2 Å resolution. The BLOC-3 complex consists of one copy of HPS1 and HPS4, which tightly associate with each other via their longin domains (LD1 and LD3). The unique four-helical bundle (4HB) domain of HPS1 is involved in stabilizing its LD1 and LD2 domains. Moreover, we identify interactions between BLOC-3 and the small GTPases RAB32/38 and RAB9A, which are essential for lysosome-related organelle biogenesis. Functional assays using zebrafish models confirm the significance of BLOC-3 assembly and its interaction with RAB9A during melanosome biogenesis. Most importantly, our structural information provides an accurate prediction for clinical variants associated with HPS. In summary, our study provides a comprehensive understanding of the molecular architecture and functional roles of BLOC-3, shedding light on HPS pathogenesis.
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Human Disease / Model
Sequence Targeting Reagents
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Mapping