Clem Jones Centre for Ageing Dementia Research, Queensland Brain Institute, The University of Queensland, Brisbane, QLD, Australia.
Queensland Brain Institute, The University of Queensland, Brisbane, QLD, Australia.
EMBO J. 2023 Jul 3;42(13):e112095. doi: 10.15252/embj.2022112095. Epub 2023 May 25.
The unique nerve terminal targeting of botulinum neurotoxin type A (BoNT/A) is due to its capacity to bind two receptors on the neuronal plasma membrane: polysialoganglioside (PSG) and synaptic vesicle glycoprotein 2 (SV2). Whether and how PSGs and SV2 may coordinate other proteins for BoNT/A recruitment and internalization remains unknown. Here, we demonstrate that the targeted endocytosis of BoNT/A into synaptic vesicles (SVs) requires a tripartite surface nanocluster. Live-cell super-resolution imaging and electron microscopy of catalytically inactivated BoNT/A wildtype and receptor-binding-deficient mutants in cultured hippocampal neurons demonstrated that BoNT/A must bind coincidentally to a PSG and SV2 to target synaptic vesicles. We reveal that BoNT/A simultaneously interacts with a preassembled PSG-synaptotagmin-1 (Syt1) complex and SV2 on the neuronal plasma membrane, facilitating Syt1-SV2 nanoclustering that controls endocytic sorting of the toxin into synaptic vesicles. Syt1 CRISPRi knockdown suppressed BoNT/A- and BoNT/E-induced neurointoxication as quantified by SNAP-25 cleavage, suggesting that this tripartite nanocluster may be a unifying entry point for selected botulinum neurotoxins that hijack this for synaptic vesicle targeting.
肉毒神经毒素 A 型(BoNT/A)独特的神经末梢靶向性是由于其能够结合神经元质膜上的两种受体:多唾液酸神经节苷脂(PSG)和突触小体糖蛋白 2(SV2)。PSGs 和 SV2 是否以及如何协调其他蛋白质参与 BoNT/A 的募集和内化仍然未知。在这里,我们证明 BoNT/A 靶向内吞进入突触小泡(SVs)需要一个三联体表面纳米簇。在培养的海马神经元中对催化失活的 BoNT/A 野生型和受体结合缺陷突变体进行活细胞超分辨率成像和电子显微镜研究表明,BoNT/A 必须巧合地与 PSG 和 SV2 结合以靶向突触小泡。我们揭示了 BoNT/A 同时与神经元质膜上预先组装的 PSG-突触融合蛋白 1(Syt1)复合物和 SV2 相互作用,促进 Syt1-SV2 纳米簇的形成,从而控制毒素进入突触小泡的内吞分拣。Syt1 CRISPRi 敲低抑制了 BoNT/A 和 BoNT/E 诱导的神经中毒,这可以通过 SNAP-25 切割来定量,这表明这个三联体纳米簇可能是一种统一的进入点,用于劫持这种进入点的选定肉毒神经毒素来靶向突触小泡。