Publications by authors named "Tania L Eskin"
Lowe Syndrome is a developmental disorder characterized by eye, kidney, and neurological pathologies, and is caused by mutations in the phosphatidylinositol-5-phosphatase OCRL. OCRL plays diverse roles in endocytic and endolysosomal trafficking, cytokinesis, and ciliogenesis, but it is unclear which of these cellular functions underlie specific patient symptoms. Here, we show that mutation of Drosophila OCRL causes cell-autonomous activation of hemocytes, which are macrophage-like cells of the innate immune system.
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- Autoinhibitory interactions between the SH3 and F-BAR domains of F-BAR proteins regulate membrane remodeling, but the structural basis of this autoregulation and its effect on cellular interactions are not well understood.
- The study utilized single-particle electron microscopy to analyze the F-BAR protein Nervous Wreck (Nwk) in soluble and membrane-bound forms, revealing that the SH3 domains reposition rather than fully detach upon membrane binding.
- Findings indicate that Nwk's autoregulation limits the activity of SH3 domains in actin filament assembly and affects synaptic growth and organization in Drosophila neurons, suggesting a coordinated relationship between membrane interactions and SH3 domain functions.
Article Synopsis
- F-BAR domain proteins are crucial for sensing and shaping membrane curvature by interacting with specific negatively charged lipids but how these interactions are controlled is not well understood.
- * In this study, researchers found that the Drosophila Nervous Wreck (Nwk) protein uses a C-terminal SH3 domain to autoregulate its own F-BAR domain, impacting how it interacts with membranes.
- * Autoregulation does not simply act as a switch; instead, it enhances Nwk's ability to form higher-order structures and affects membrane deformation, depending on the negative charge of the membrane composition.*