Restructuring of the plasma membrane upon damage by LC3-associated macropinocytosis

Research output: Contribution to journalJournal articleResearchpeer-review


  • Stine Lauritzen Sønder
  • Swantje Christin Häger
  • Anne Sofie Busk Heitmann
  • Frankel, Lisa
  • Catarina Dias
  • Adam Cohen Simonsen
  • Jesper Nylandsted

The plasma membrane shapes and protects the eukaryotic cell from its surroundings and is crucial for cell life. Although initial repair mechanisms to reseal injured membranes are well established, less is known about how cells restructure damaged membranes in the aftermath to restore homeostasis. Here, we show that cells respond to plasma membrane injury by activating proteins associated with macropinocytosis specifically at the damaged membrane. Subsequent to membrane resealing, cells form large macropinosomes originating from the repair site, which eventually become positive for autophagy-related LC3B protein. This process occurs independent of ULK1, ATG13, and WIPI2 but dependent on ATG7, p62, and Rubicon. Internalized macropinosomes shrink in the cytoplasm, likely by osmotic draining, and eventually fuse with lysosomes. We propose that a form of macropinocytosis coupled to noncanonical autophagy, which we term LC3-associated macropinocytosis (LAM) functions to remove damaged material from the plasma membrane and restore membrane integrity upon injury.

Original languageEnglish
Article numbereabg1969
JournalScience Advances
Issue number27
Publication statusPublished - 2021

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© 2021 The Authors, some rights reserved; exclusive licensee American Association for the Advancement of Science.

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