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Lysosomal Hydrolases

Lysosomal Hydrolases

Lysosomes are the site for the degradation of macromolecules and biological polymers released during membrane trafficking events such as secretory, endocytic, autophagic, and phagocytic pathways. The membrane-enclosed area of the lysosome, called the lumen, contains hydrolytic enzymes active in an acidic environment. These acid hydrolases are functional at a pH between 4.5 and 5 and are involved in cellular processes such as cell signaling, energy metabolism, restoration of the plasma membrane,...

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In Vitro Aggregation Assays Using Hyperphosphorylated Tau Protein

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Published on: January 2, 2015

A decrease in Fkbp52 alters autophagosome maturation and A152T-tau clearance in vivo.

Emilie Lesport^1,2, Lucie Commeau¹, Mélanie Genet¹

¹Institut Professeur Baulieu, INSERM U1195, Kremlin-Bicêtre, France.

Frontiers in Cellular Neuroscience

|August 9, 2024

Summary

This summary is machine-generated.

Reduced FKBP52 protein impairs lysosome and autophagosome transport in neurons. This hinders the clearance of toxic Tau proteins, exacerbating tauopathy pathogenesis.

Keywords:

FKBP52 autophagy lysosomes tau tauopathies zebrafish

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Area of Science:

Neuroscience
Cell Biology
Genetics

Background:

Autophagy-lysosomal pathway dysfunction worsens tauopathies.
FKBP52 protein interacts with Tau and is reduced in affected brains.
FKBP52 is vital for neuronal lysosomal function and Tau clearance.

Purpose of the Study:

Investigate FKBP52's role in axonal transport and autophagy in vivo.
Determine if FKBP52 deficiency impacts pathogenic Tau clearance.

Main Methods:

Generated zebrafish *fkbp4* loss-of-function mutants.
Assessed Lamp1 vesicle trafficking and autophagic flux using transgenic lines.
Examined clearance of A152T-Tau in *fkbp4* mutant zebrafish.

Main Results:

*fkbp4* mutants exhibit altered axonal transport of Lamp1 vesicles.
Autophagic flux is impaired in *fkbp4* mutant embryos.
Clearance of pathogenic A152T-Tau is slower in *fkbp4* heterozygous mutants.

Conclusions:

FKBP52 is essential for lysosome and autophagosome trafficking and maturation along axons.
Reduced FKBP52 hinders pathogenic Tau clearance in vivo, contributing to tauopathy.