Pseudomonas species export the amyloid-forming protein FapC to strengthen bacterial biofilm. P. species also produce the biosurfactant rhamnolipid (Rhl) and its outer membrane contains lipopolysaccharide (LPS). Given the possible contacts between FapC, Rhl and LPS, we here investigate how Rhl and LPS affect FapC fibrillation compared with SDS, known to promote fibrillation of proteins at sub-micellar concentrations. Micelles of all three surfactants help FapC bypass the nucleation lag phase, leading to rapid fibrillation, which persists even at high concentrations of micelles and incorporates almost all available FapC monomers. Fibrils formed at high micellar concentrations of Rhl and SDS seed fibrillation at low surfactant concentrations while retaining the original fibril structure. FapC interacts strongly with SDS to form a dense network of narrow fibrils. Small angle X-ray scattering (SAXS) analyses reveal that surfactants reduce the population of intermediates in the fibrillation process and detect a fast aggregation step over the first 2-4 h which precedes the main fibrillation monitored by Thioflavin T. An additional SAXS-detected rearrangement of early aggregates occurs after 4-10 h. At high Rhl concentrations, the micelles are decorated with protein fibrils. SDS induces FapC fibrillation so efficiently that epigallocatechin-3-gallate (EGCG) is unable to inhibit this process. However, EGCG stimulates FapC oligomer formation and inhibits fibrillation both on its own and in the presence of Rhl and LPS. This oligomer could be modelled as a compact core with a flexible shell. This suggests that EGCG can override the natural amyloid-stimulatory properties of these biosurfactants and thus target biofilm.

中文翻译：

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细菌两亲物作为淀粉样蛋白诱导剂：鼠李糖脂和脂多糖对FapC纤颤的影响。

假单胞菌种输出淀粉样蛋白FapC以增强细菌生物膜。体育种还产生生物表面活性剂鼠李糖脂（Rhl），其外膜含有脂多糖（LPS）。考虑到FapC，Rhl和LPS之间可能存在的联系，我们在这里研究Rhl和LPS与SDS相比如何影响FapC的原纤维形成，而SDS已知会在亚胶束浓度下促进蛋白质的原纤化。所有这三种表面活性剂的胶束都有助于FapC绕过成核滞后阶段，从而导致快速原纤化，即使在高浓度的胶束下也能持续原纤化，并掺入了几乎所有可用的FapC单体。高胶束浓度的Rhl和SDS在低表面活性剂浓度下形成原纤维，同时保留了原纤维结构。FapC与SDS强烈相互作用，形成狭窄的原纤维密集网络。小角度X射线散射（SAXS）分析表明，表面活性剂减少了原纤化过程中的中间体数量，并在最初的2-4小时内检测到快速的聚集步骤，此步骤在硫黄素T监测主要的原纤化之前。早期聚集体的重排在4-10小时后发生。在高Rhl浓度下，胶束被蛋白原纤维修饰。SDS如此有效地诱导FapC纤颤，以致表没食子儿茶素-3-没食子酸酯（EGCG）无法抑制该过程。但是，EGCG本身或在Rhl和LPS的存在下都刺激FapC低聚物的形成并抑制原纤维形成。可以将该低聚物建模为具有柔性壳的紧凑型核。