A role for tropomyosins in activity-dependent bulk endocytosis?

Rachel Gormal, Nicholas Valmas, Thomas Fath, Frederic Meunier*

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

4 Citations (Scopus)
19 Downloads (Pure)


Bulk endocytosis allows stimulated neurons to take up a large portion of the presynaptic plasma membrane in order to regenerate synaptic vesicle pools. Actin, one of the most abundant proteins in eukaryotic cells, plays an important role in this process, but a detailed mechanistic understanding of the involvement of the cortical actin network is still lacking, in part due to the relatively small size of nerve terminals and the limitation of optical microscopy. We recently discovered that neurosecretory cells display a similar, albeit much larger, form of bulk endocytosis in response to secretagogue stimulation. This allowed us to identify a novel highly dynamic role for the acto-myosin II cortex in generating constricting rings that precede the fission of nascent bulk endosomes. In this review we focus on the mechanism underpinning this dramatic switch in the organization and function of the cortical actin network. We provide additional experimental data that suggest a role of tropomyosin Tpm3.1 and Tpm4.2 in this process, together with an emerging model of how actin controls bulk endocytosis.

Original languageEnglish
Pages (from-to)112-118
Number of pages7
JournalMolecular and Cellular Neuroscience
Publication statusPublished - 1 Oct 2017
Externally publishedYes

Bibliographical note

Copyright the Author(s) 2017. Version archived for private and non-commercial use with the permission of the author/s and according to publisher conditions. For further rights please contact the publisher.


  • Bulk endocytosis
  • Cortical actin network
  • Cytoskeleton
  • Exocytosis
  • Myosin II
  • Tropomyosin


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