Role for formin-like 1-dependent acto-myosin assembly in lipid droplet dynamics and lipid storage

Simon G. Pfisterer, Gergana Gateva, Peter Horvath, Juho Pirhonen, Veijo T. Salo, Leena Karhinen, Markku Varjosalo, Samppa J. Ryhänen, Pekka Lappalainen and Elina Ikonen ()
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Simon G. Pfisterer: Faculty of Medicine, University of Helsinki
Gergana Gateva: Institute of Biotechnology, University of Helsinki
Peter Horvath: Institute for Molecular Medicine Finland (FIMM), University of Helsinki
Juho Pirhonen: Faculty of Medicine, University of Helsinki
Veijo T. Salo: Faculty of Medicine, University of Helsinki
Leena Karhinen: Faculty of Medicine, University of Helsinki
Markku Varjosalo: Institute of Biotechnology, University of Helsinki
Samppa J. Ryhänen: Children’s Hospital, Helsinki University Central Hospital and University of Helsinki
Pekka Lappalainen: Institute of Biotechnology, University of Helsinki
Elina Ikonen: Faculty of Medicine, University of Helsinki

Nature Communications, 2017, vol. 8, issue 1, 1-14

Abstract: Abstract Lipid droplets (LDs) are cellular organelles specialized in triacylglycerol (TG) storage undergoing homotypic clustering and fusion. In non-adipocytic cells with numerous LDs this is balanced by poorly understood droplet dissociation mechanisms. We identify non-muscle myosin IIa (NMIIa/MYH-9) and formin-like 1 (FMNL1) in the LD proteome. NMIIa and actin filaments concentrate around LDs, and form transient foci between dissociating LDs. NMIIa depletion results in decreased LD dissociations, enlarged LDs, decreased hydrolysis and increased storage of TGs. FMNL1 is required for actin assembly on LDs in vitro and for NMIIa recruitment to LDs in cells. We propose a novel acto-myosin structure regulating lipid storage: FMNL1-dependent assembly of myosin II-functionalized actin filaments on LDs facilitates their dissociation, thereby affecting LD surface-to-volume ratio and enzyme accessibility to TGs. In neutrophilic leucocytes from MYH9-related disease patients NMIIa inclusions are accompanied by increased lipid storage in droplets, suggesting that NMIIa dysfunction may contribute to lipid imbalance in man.

Date: 2017
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DOI: 10.1038/ncomms14858

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