Type II phosphatidylinositol 4-kinases function sequentially in cargo delivery from early endosomes to melanosomes.


Journal

The Journal of cell biology
ISSN: 1540-8140
Titre abrégé: J Cell Biol
Pays: United States
ID NLM: 0375356

Informations de publication

Date de publication:
07 11 2022
Historique:
received: 20 10 2021
revised: 31 03 2022
accepted: 04 05 2022
entrez: 28 9 2022
pubmed: 29 9 2022
medline: 1 10 2022
Statut: ppublish

Résumé

Melanosomes are pigment cell-specific lysosome-related organelles in which melanin pigments are synthesized and stored. Melanosome maturation requires delivery of melanogenic cargoes via tubular transport carriers that emanate from early endosomes and that require BLOC-1 for their formation. Here we show that phosphatidylinositol-4-phosphate (PtdIns4P) and the type II PtdIns-4-kinases (PI4KIIα and PI4KIIβ) support BLOC-1-dependent tubule formation to regulate melanosome biogenesis. Depletion of either PI4KIIα or PI4KIIβ with shRNAs in melanocytes reduced melanin content and misrouted BLOC-1-dependent cargoes to late endosomes/lysosomes. Genetic epistasis, cell fractionation, and quantitative live-cell imaging analyses show that PI4KIIα and PI4KIIβ function sequentially and non-redundantly downstream of BLOC-1 during tubule elongation toward melanosomes by generating local pools of PtdIns4P. The data show that both type II PtdIns-4-kinases are necessary for efficient BLOC-1-dependent tubule elongation and subsequent melanosome contact and content delivery during melanosome biogenesis. The independent functions of PtdIns-4-kinases in tubule extension are downstream of likely redundant functions in BLOC-1-dependent tubule initiation.

Identifiants

pubmed: 36169639
pii: 213509
doi: 10.1083/jcb.202110114
pmc: PMC9524207
pii:
doi:

Substances chimiques

Intracellular Signaling Peptides and Proteins 0
Melanins 0
Phosphatidylinositol Phosphates 0
phosphatidylinositol 4-phosphate 0
1-Phosphatidylinositol 4-Kinase EC 2.7.1.67

Types de publication

Journal Article Research Support, Non-U.S. Gov't Research Support, N.I.H., Extramural

Langues

eng

Sous-ensembles de citation

IM

Subventions

Organisme : Centre National de la Recherche Scientifique
Organisme : Genespoir
Organisme : Institut Curie
Organisme : NEI NIH HHS
ID : R01 EY015625
Pays : United States
Organisme : Institut National de la Santé et de la Recherche Médicale

Informations de copyright

© 2022 Zhu et al.

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Auteurs

Yueyao Zhu (Y)

Department of Pathology and Laboratory Medicine, Children's Hospital of Philadelphia Research Institute, Philadelphia, PA.
Department of Biology, University of Pennsylvania School of Arts and Sciences, Philadelphia, PA.

Shuixing Li (S)

Department of Pathology and Laboratory Medicine, Children's Hospital of Philadelphia Research Institute, Philadelphia, PA.
Department of Pathology and Laboratory Medicine and Department of Physiology, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA.

Alexa Jaume (A)

Department of Pathology and Laboratory Medicine, Children's Hospital of Philadelphia Research Institute, Philadelphia, PA.
Department of Pathology and Laboratory Medicine and Department of Physiology, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA.

Riddhi Atul Jani (RA)

Institut Curie, PSL Research University, CNRS, UMR 144, Structure and Membrane Compartments, Paris, France.

Cédric Delevoye (C)

Institut Curie, PSL Research University, CNRS, UMR 144, Structure and Membrane Compartments, Paris, France.

Graça Raposo (G)

Institut Curie, PSL Research University, CNRS, UMR 144, Structure and Membrane Compartments, Paris, France.

Michael S Marks (MS)

Department of Pathology and Laboratory Medicine, Children's Hospital of Philadelphia Research Institute, Philadelphia, PA.
Department of Pathology and Laboratory Medicine and Department of Physiology, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA.

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Classifications MeSH