RESTORATION HARDWARE: During interphase, mammalian cells have low membrane tension, and clathrin-mediated endocytosis (CME) proceeds normally with no special need for actin (1). During mitosis, membrane tension is high, the actin (purple) is sequestered at the cell cortex, and CME can’t proceed because actin is required to help stretch the clathrin-coated pits to form full vesicles (2). Freeing up some of the actin during mitosis allows the protein to help form clathrin-coated vesicles, restoring CME
(3).© KIMBERLY BATTISTA
The paper
S. Kaur et al., “An unmet actin requirement explains the mitotic inhibition of clathrin-mediated endocytosis,” eLife, 3:e00829, 2014.
For decades, scientists observed clathrin-mediated endocytosis (CME)—the process of forming vesicles to pull protein cargo into a cell—ceasing during mitosis in mammalian cells. But they didn’t know why. From prophase to anaphase, shallow clathrin-coated pits form at the plasma membrane, but the cell never internalizes them.
Two main theories have tried to explain how endocytosis is inhibited. After finding that proteins involved in endocytosis are phosphorylated during mitosis, researchers proposed that phosphorylation of crucial components turns off CME. The second theory suggested that elevated tension in the plasma membrane prevents clathrin-coated pits from pinching off into closed vesicles. But scientists had not reached a consensus.
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