Answers are grounded in this paper and cite their sources.
In vitro study reveals calcium-dependent dual binding of annexin A11 C-terminal domain to RNA and lipid vesicles, highlighting mechanisms of neuronal RNA trafficking.
Intracellular RNA transport is a key process for neuronal function, yet the molecular mechanisms underlying RNA tethering to organelles remain poorly understood. Annexin A11 (ANXA11) has been proposed as a tether linking RNA granules to lysosomes, but the specific role of its C-terminal domain (Ct) has remained unclear. Here, we provide direct biochemical evidence that the ANXA11 Ct directly binds lipid vesicles and RNA simultaneously. Using a combination of pull-down assays, microscale thermophoresis, and fluorescence-based approaches, we quantified the binding affinities of the Ct for phospholipid vesicles and RNA and demonstrated that these interactions are strictly Ca 2+ -dependent. Small-angle X-ray scattering and molecular dynamics simulations reveal that Ca 2+ induces conformational changes in the Ct, modulating its conformational heterogeneity and redistributing surface properties, thereby exposing a membrane-binding face opposite to the Ca 2+ -coordinating RNA-binding loops. Pull-down assays with neutral micelles suggested that membrane engagement requires both hydrophobic and ionic interactions. These findings challenge the classical view that RNA binding is restricted to the N-terminal domain and that the Ct engages membrane exclusively. Our data establish the Ct as a Ca 2+ -regulated domain, capable of simultaneously coordinating RNA and membrane interactions, providing a mechanistic framework for ANXA11-mediated RNA hitchhiking and intracellular RNA trafficking in neurons.
No takes yet. Share an insight, caveat, or question.
Alfurno et al. (2026) studied this question.
Synapse has enriched 10 related papers. Consider them for comparative context: