CDC50A is required for aminophospholipid transport and cell fusion in mouse C2C12 myoblasts

Marta Grifell-Junyent, Julia F. Baum, Silja Valimets, Andreas Herrmann, Coen C. Paulusma, Rosa L. Lopez-Marques, Thomas Gunther Pomorski

Research output: Contribution to journalArticleAcademicpeer-review


Myoblast fusion is essential for the formation of multinucleated muscle fibers and is promoted by transient changes in the plasma membrane lipid distribution. However, little is known about the lipid transporters regulating these dynamic changes. Here, we show that proliferating myoblasts exhibit an aminophospholipid flippase activity that is downregulated during differentiation. Deletion of the P4-ATPase flippase subunit CDC50A (also known as TMEM30A) results in loss of the aminophospholipid flippase activity and compromises actin remodeling, RAC1 GTPase membrane targeting and cell fusion. In contrast, deletion of the P4-ATPase ATP11A affects aminophospholipid uptake without having a strong impact on cell fusion. Our results demonstrate that myoblast fusion depends on CDC50A and may involve multiple CDC50A-dependent P4-ATPases that help to regulate actin remodeling.
Original languageEnglish
Article numberjcs258649
JournalJournal of Cell Science
Issue number5
Publication statusPublished - 1 Mar 2022


  • Aminophospholipid translocase
  • Myogenesis
  • P4-ATPase
  • Phospholipid
  • Skeletal myoblasts

Cite this