Publication Date

1-1-2025

Journal

Protein Scoemce

DOI

10.1002/pro.5249

PMID

39660930

PMCID

PMC11633055

PubMedCentral® Posted Date

12-11-2024

PubMedCentral® Full Text Version

Post-print

Abstract

Intracellular lipid binding proteins (iLBPs) play crucial roles in lipid transport and cellular metabolism across the animal kingdom. Recently, a fat‐to‐neuron axis was described in Caenorhabditis elegans, in which lysosomal activity in the fat liberates polyunsaturated fatty acids (PUFAs) that signal to neurons and extend lifespan with durable fecundity. In this study, we investigate the structure and binding mechanisms of a lifespan‐extending lipid chaperone, lipid binding protein‐3 (LBP‐3), which shuttles dihomo‐γ‐linolenic (DGLA) acid from intestinal fat to neurons. We present the first high‐resolution crystal structure of LBP‐3, which reveals a classic iLBP fold with an unexpected and unique homodimeric arrangement via interstrand interactions that is incompatible with ligand binding. We identify key ionic interactions that mediate DGLA binding within the lipid binding pocket. Molecular dynamics simulations further elucidate LBP‐3's preferential binding to DGLA due to its rotational freedom and access to favorable binding conformations compared to other 20‐carbon PUFAs. We also propose that LBP‐3 dimerization may be a unique regulatory mechanism for lipid chaperones.

Keywords

Animals, Caenorhabditis elegans, Caenorhabditis elegans Proteins, Molecular Dynamics Simulation, Fatty Acids, Unsaturated, Crystallography, X-Ray, Protein Binding, Fatty Acid-Binding Proteins, biochemistry, in silico docking, lipid signaling, longevity, molecular dynamics, protein engineering, structural biology

Published Open-Access

yes

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