Department of Physics, University of California, Merced, CA 95343.
Laboratory of Single Molecule Biophysics, National Heart, Lung and Blood Institute, NIH, Bethesda, MD 20892.
Proc Natl Acad Sci U S A. 2023 Jan 17;120(3):e2212507120. doi: 10.1073/pnas.2212507120. Epub 2023 Jan 10.
Intracellular cargos are often membrane-enclosed and transported by microtubule-based motors in the presence of microtubule-associated proteins (MAPs). Whereas increasing evidence reveals how MAPs impact the interactions between motors and microtubules, critical questions remain about the impact of the cargo membrane on transport. Here we combined in vitro optical trapping with theoretical approaches to determine the effect of a lipid cargo membrane on kinesin-based transport in the presence of MAP tau. Our results demonstrate that attaching kinesin to a fluid lipid membrane reduces the inhibitory effect of tau on kinesin. Moreover, adding cholesterol, which reduces kinesin diffusion in the cargo membrane, amplifies the inhibitory effect of tau on kinesin binding in a dosage-dependent manner. We propose that reduction of kinesin diffusion in the cargo membrane underlies the effect of cholesterol on kinesin binding in the presence of tau, and we provide a simple model for this proposed mechanism. Our study establishes a direct link between cargo membrane cholesterol and MAP-based regulation of kinesin-1. The cholesterol effects uncovered here may more broadly extend to other lipid alterations that impact motor diffusion in the cargo membrane, including those associated with aging and neurological diseases.
细胞内货物通常被膜包裹,并在微管相关蛋白 (MAP) 的存在下由基于微管的马达运输。虽然越来越多的证据揭示了 MAP 如何影响马达和微管之间的相互作用,但关于货物膜对运输的影响仍存在关键问题。在这里,我们将体外光学捕获与理论方法相结合,以确定脂质货物膜在存在 MAP tau 的情况下对基于驱动蛋白的运输的影响。我们的结果表明,将驱动蛋白附着到流体脂质膜上会降低 tau 对驱动蛋白的抑制作用。此外,添加胆固醇会降低货物膜中驱动蛋白的扩散,从而以剂量依赖的方式放大 tau 对驱动蛋白结合的抑制作用。我们提出,在 tau 存在下,货物膜中驱动蛋白扩散的减少是胆固醇对驱动蛋白结合影响的基础,并为此提出的机制提供了一个简单的模型。我们的研究建立了货物膜胆固醇和基于 MAP 的驱动蛋白-1 调节之间的直接联系。在这里揭示的胆固醇作用可能更广泛地扩展到其他影响货物膜中马达扩散的脂质改变,包括与衰老和神经疾病相关的改变。