Filamin FLN-2 promotes MVB biogenesis by mediating vesicle docking on the actin cytoskeleton

J Cell Biol. 2022 Jul 4;221(7):e202201020. doi: 10.1083/jcb.202201020. Epub 2022 May 16.

Abstract

Multivesicular bodies (MVBs) contain intralumenal vesicles that are delivered to lysosomes for degradation or released extracellularly for intercellular signaling. Here, we identified Caenorhabditis elegans filamin FLN-2 as a novel regulator of MVB biogenesis. FLN-2 co-localizes with V-ATPase subunits on MVBs, and the loss of FLN-2 affects MVB biogenesis, reducing the number of MVBs in C. elegans hypodermis. FLN-2 associates with actin filaments and is required for F-actin organization. Like fln-2(lf) mutation, inactivation of the V0 or V1 sector of V-ATPase or inhibition of actin polymerization impairs MVB biogenesis. Super-resolution imaging shows that FLN-2 docks V-ATPase-decorated MVBs onto actin filaments. FLN-2 interacts via its calponin-homology domains with F-actin and the V1-E subunit, VHA-8. Our data suggest that FLN-2 mediates the docking of MVBs on the actin cytoskeleton, which is required for MVB biogenesis.

Publication types

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

MeSH terms

  • Actin Cytoskeleton* / metabolism
  • Actins / metabolism
  • Animals
  • Caenorhabditis elegans Proteins* / genetics
  • Caenorhabditis elegans Proteins* / metabolism
  • Caenorhabditis elegans* / genetics
  • Caenorhabditis elegans* / metabolism
  • Filamins* / genetics
  • Filamins* / metabolism
  • Multivesicular Bodies* / metabolism
  • Vacuolar Proton-Translocating ATPases / metabolism

Substances

  • Actins
  • Caenorhabditis elegans Proteins
  • Filamins
  • Vacuolar Proton-Translocating ATPases