AI Article Synopsis
- Membrane budding is critical for cell survival, transforming flat membranes into vesicles, with coat-proteins like clathrin identified as key players, but many non-coated budding mechanisms remain poorly understood.
- Research utilizing live neuroendocrine cells and protein modeling reveals that actin filaments and dynamin work together to shape the membrane, first forming a Λ-profile and then constricting it into vesicles.
- This discovery of how non-coated membrane budding operates expands our understanding of membrane dynamics, suggesting that the roles of dynamin and actin are more versatile and impactful across various cell types than previously believed.
Article Abstract
Membrane budding entails forces to transform flat membrane into vesicles essential for cell survival. Accumulated studies have identified coat-proteins (e.g., clathrin) as potential budding factors. However, forces mediating many non-coated membrane buddings remain unclear. By visualizing proteins in mediating endocytic budding in live neuroendocrine cells, performing in vitro protein reconstitution and physical modeling, we discovered how non-coated-membrane budding is mediated: actin filaments and dynamin generate a pulling force transforming flat membrane into Λ-shape; subsequently, dynamin helices surround and constrict Λ-profile's base, transforming Λ- to Ω-profile, and then constrict Ω-profile's pore, converting Ω-profiles to vesicles. These mechanisms control budding speed, vesicle size and number, generating diverse endocytic modes differing in these parameters. Their impact is widespread beyond secretory cells, as the unexpectedly powerful functions of dynamin and actin, previously thought to mediate fission and overcome tension, respectively, may contribute to many dynamin/actin-dependent non-coated-membrane buddings, coated-membrane buddings, and other membrane remodeling processes.
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| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC9237132 | PMC |
| http://dx.doi.org/10.1038/s41467-022-31286-4 | DOI Listing |
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