Journal
SCIENCE ADVANCES
Volume 6, Issue 50, Pages -Publisher
AMER ASSOC ADVANCEMENT SCIENCE
DOI: 10.1126/sciadv.aba5783
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Funding
- National Key Research and Development Program of China [2016YFA0501000]
- National Natural Science Foundation of China [81821091, 31501128, 31490592, 31871039, 81761138044, 81527901, 81801330, 91832000]
- Key Research and Development Program of Zhejiang Province [2020C03009]
- Science and Technology Planning Project of Guangdong Province [2018B030331001]
- Key Realm R&D Program of Guangdong Province [2019B030335001]
- Chinese Ministry of Education Project 111 Program [B13026]
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Organelle transport requires dynamic cytoskeleton remodeling, but whether cytoskeletal dynamics are, in turn, regulated by organelles remains elusive. Here, we demonstrate that late endosomes, a type of prelysosomal organelles, facilitate actin-cytoskeleton remodeling via cytosolic translocation of immature protease cathepsin D (cathD) during microglia migration. After cytosolic translocation, late endosome-derived cathD juxtaposes actin filaments at the leading edge of lamellipodia. Suppressing cathD expression or blocking its cytosolic translocation impairs the maintenance but not the initiation of lamellipodial extension. Moreover, immature cathD balances the activity of the actin-severing protein cofilin to maintain globular-actin (G-actin) monomer pool for local actin recycling. Our study identifies cathD as a key lysosomal molecule that unconventionally contributes to actin cytoskeleton remodeling via cytosolic translocation during adenosine triphosphate-evoked microglia migration.
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