ArticleThe Journal of cell biology2026
MIM triggers formin to Arp2/3-based actin assembly in membrane remodeling in Drosophila embryos.
Article in The Journal of cell biology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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6 authors.
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Abstract
BAR domain-containing proteins are key regulators of endocytosis and actin remodeling. Their function in morphogenesis remains to be investigated. We report that the I-BAR domain-containing protein, missing-in-metastasis (MIM) (also called MTSS1), promotes branched actin network formation and endocytosis to drive rapid, cyclical plasma membrane remodeling during syncytial divisions in Drosophila embryos. Actin-rich villous protrusions in the apical caps in interphase are depleted in metaphase, concurrent with furrow extension between adjacent nuclei. MIM depletion results in a loss of furrow extension and in longer, more abundant apical protrusions containing the formin diaphanous. Branched actin networks promoted by MIM are in balance with bundled actin networks induced by RhoGEF2 and diaphanous. Cyclical recruitment of MIM to the cortex promotes localization of active Rac, the WAVE regulatory complex, and the Arp2/3 complex to drive endocytic membrane remodeling. These findings identify MIM as an integrator of actin and endocytic dynamics that enables rapid membrane remodeling during Drosophila syncytial division cycles.
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