Category Ranking

98%

Total Visits

921

Avg Visit Duration

2 minutes

Citations

20

Article Abstract

Adaptor protein complex-3 (AP-3) mediates cargo sorting from endosomes to lysosomes and lysosome-related organelles. Recently, it was shown that AP-3 adopts a constitutively open conformation compared to the related AP-1 and AP-2 coat complexes, which are inactive until undergoing large conformational changes upon membrane recruitment. How AP-3 is regulated is therefore an open question. To understand the mechanism of AP-3 membrane recruitment and activation, we reconstituted human AP-3 and determined multiple structures in the soluble and membrane-bound states using electron cryo-microscopy. Similar to yeast AP-3, human AP-3 is in a constitutively open conformation. To reconstitute AP-3 activation by adenosine di-phosphate (ADP)-ribosylation factor 1 (Arf1), a small guanosine tri-phosphate (GTP)ase, we used lipid nanodiscs to build Arf1-AP-3 complexes on membranes and determined three structures showing the stepwise conformational changes required for formation of AP-3 coated vesicles. First, membrane recruitment is driven by one of two predicted Arf1 binding sites, which flexibly tethers AP-3 to the membrane. Second, cargo binding causes AP-3 to adopt a fixed position and rigidifies the complex, which stabilizes binding for a second Arf1 molecule. Finally, binding of the second Arf1 molecule provides the template for AP-3 dimerization, providing a glimpse into the first step of coat polymerization. We propose coat polymerization only occurs after cargo engagement, thereby linking cargo sorting with assembly of higher-order coat structures. Additionally, we provide evidence for two amphipathic helices in AP-3, suggesting that AP-3 contributes to membrane deformation during coat assembly. In total, these data provide evidence for the first stages of AP-3-mediated vesicle coat assembly.

Download full-text PDF

Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC11670113PMC
http://dx.doi.org/10.1073/pnas.2411974121DOI Listing

Publication Analysis

Top Keywords

ap-3
15
membrane recruitment
12
ap-3 coated
8
cargo sorting
8
constitutively open
8
open conformation
8
conformational changes
8
ap-3 membrane
8
human ap-3
8
binding second
8

Similar Publications

The diagnostic approaches for Hermansky-Pudlak Syndrome (HPS) include genetic sequencing, immunoblotting, electron microscopy (EM), and flow cytometry with mepacrine staining. However, these methods are often impractical for routine clinical use due to high cost, technical complexity, and limited availability. In this study, we evaluated dense granules (DGs) function in HPS mouse models using flow cytometry with mepacrine and FluoZin-3 staining.

View Article and Find Full Text PDF

Therapeutic plasma exchange (TPE) is used to lower triglyceride levels in patients with severe hypertriglyceridemia-associated acute pancreatitis (HTG-AP). However, evidence supporting the effectiveness of TPE in preventing end-organ damage remains limited. This retrospective cohort study was conducted using the TriNetX database to evaluate adults with acute pancreatitis, triglyceride levels > 1000 mg/dL, and "worrisome criteria", defined as clinical indicators of disease severity such as fever, leukocytosis, elevated lactate, or signs of shock.

View Article and Find Full Text PDF

A Set of Fluorescent Protein-Based Markers for Major Vesicle Coat Proteins in Yeast.

Membranes (Basel)

July 2025

State Key Laboratory of Microbial Metabolism, Ministry of Education Key Laboratory for the Genetics of Developmental and Neuropsychiatric Disorders, and Joint International Research Laboratory of Metabolic & Developmental Sciences, School of Life Sciences and Biotechnology, Shanghai Jiao Tong Univer

In eukaryotic cells, vesicle-mediated transport interconnects the endomembrane system. These vesicles are formed by coat proteins via deformation of donor membranes. Here, we constructed a set of fluorescent protein-based markers for major coat protein complexes in the yeast model system, and examined their subcellular localization patterns.

View Article and Find Full Text PDF

Lysosome damage activates multiple pathways to prevent lysosome-dependent cell death, including a repair mechanism involving endoplasmic reticulum (ER)-lysosome membrane contact sites, phosphatidylinositol 4-kinase-2a (PI4K2A), phosphatidylinositol-4 phosphate (PI4P), and oxysterol-binding protein-like proteins (OSBPLs) lipid transfer proteins. PI4K2A localizes to the trans-Golgi network and endosomes, yet how it is delivered to damaged lysosomes remains unknown. During acute sterile damage and damage caused by intracellular bacteria, we show that ATG9A-containing vesicles perform a critical role in delivering PI4K2A to damaged lysosomes.

View Article and Find Full Text PDF