ArticleNature communications2025
Moesin integrates cortical and lamellar actin networks during Drosophila macrophage migration.
Article in Nature communications, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
What it found
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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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
3 citing papers in PubMed.
- A Novel MSN Mutation Impairs CD4Journal of clinical immunology · 2026Article
- External immune sentinels in the seawater ecosystem: the specialization of bivalve hemocytes.Frontiers in immunology · 2026Article
- Neuronal Actin Remodeling and Its Role in Higher Nervous Activity.International journal of molecular sciences · 2025Review
Corrections and comments
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Authors and funding
8 authors.
Funding
Abstract
Cells are thought to adopt mechanistically distinct migration modes depending on cell-type and environmental factors. These modes are assumed to be driven by mutually exclusive actin cytoskeletal organizations, which are either lamellar (flat, branched network) or cortical (crosslinked to the plasma membrane). Here we exploit Drosophila macrophage (hemocyte) developmental dispersal to reveal that these cells maintain both a lamellar actin network at their cell front and a cortical actin network at the rear. Loss of classical actin cortex regulators, such as Moesin, perturb hemocyte morphology and cell migration. Furthermore, cortical and lamellipodial actin networks are interregulated. Upon phosphorylation and binding to the plasma membrane, Moesin is advected to the rear by lamellar actin flow. Simultaneously, the cortical actin network feeds back on the lamella to help regulate actin flow speed and leading-edge dynamics. These data reveal that hemocyte motility requires both lamellipodial and cortical actin architectures in homeostatic equilibrium.
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Registered trials
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