Hitchcock-DeGregori Sarah E, Irving Thomas C
Pathology and Laboratory Medicine, Robert Wood Johnson Medical School, Rutgers University, Piscataway, New Jersey.
CSRRI and Dept. BCHS, Illinois Institute of Technology, Chicago, Illinois.
Biophys J. 2014 Oct 7;107(7):1493-501. doi: 10.1016/j.bpj.2014.07.069.
The sliding filament model of muscle contraction, put forward by Hugh Huxley and Jean Hanson in 1954, is 60 years old in 2014. Formulation of the model and subsequent proof was driven by the pioneering work of Hugh Huxley (1924-2013). We celebrate Huxley's integrative approach to the study of muscle contraction; how he persevered throughout his career, to the end of his life at 89 years, to understand at the molecular level how muscle contracts and develops force. Here we show how his life and work, with its focus on a single scientific problem, had impact far beyond the field of muscle contraction to the benefit of multiple fields of cellular and structural biology. Huxley introduced the use of x-ray diffraction to study the contraction in living striated muscle, taking advantage of the paracrystalline lattice that would ultimately allow understanding contraction in terms of single molecules. Progress required design of instrumentation with ever-increasing spatial and temporal resolution, providing the impetus for the development of synchrotron facilities used for most protein crystallography and muscle studies today. From the time of his early work, Huxley combined electron microscopy and biochemistry to understand and interpret the changes in x-ray patterns. He developed improved electron-microscopy techniques, thin sections and negative staining, that enabled answering major questions relating to the structure and organization of thick and thin filaments in muscle and the interaction of myosin with actin and its regulation. Huxley established that the ATPase domain of myosin forms the crossbridges of thick filaments that bind actin, and introduced the idea that myosin makes discrete steps on actin. These concepts form the underpinning of cellular motility, in particular the study of how myosin, kinesin, and dynein motors move on their actin and tubulin tracks, making Huxley a founder of the field of cellular motility.
1954年由休·赫胥黎(Hugh Huxley)和琼·汉森(Jean Hanson)提出的肌肉收缩滑动丝模型,到2014年已有60年历史。该模型的提出及后续验证得益于休·赫胥黎(1924 - 2013)的开创性工作。我们颂扬赫胥黎研究肌肉收缩的综合方法;他在整个职业生涯中坚持不懈,直至89岁生命终结,致力于从分子层面理解肌肉如何收缩及产生力量。在此,我们展示他专注于单一科学问题的一生及其工作,如何产生了远超肌肉收缩领域的影响,惠及细胞生物学和结构生物学的多个领域。赫胥黎引入利用X射线衍射研究活体横纹肌收缩,借助准晶体晶格,最终得以从单分子角度理解收缩过程。研究进展需要设计出空间和时间分辨率不断提高的仪器,这推动了如今用于大多数蛋白质晶体学和肌肉研究的同步加速器设施的发展。从早期工作开始,赫胥黎就将电子显微镜和生物化学结合起来以理解和解释X射线图谱的变化。他改进了电子显微镜技术,如薄切片和负染色技术,从而能够回答与肌肉中粗、细肌丝的结构和组织以及肌球蛋白与肌动蛋白的相互作用及其调节相关的主要问题。赫胥黎确定肌球蛋白的ATP酶结构域形成粗肌丝与肌动蛋白结合的横桥,并提出肌球蛋白在肌动蛋白上进行离散步移的观点。这些概念构成了细胞运动性的基础,尤其是关于肌球蛋白、驱动蛋白和动力蛋白如何在其肌动蛋白和微管蛋白轨道上移动的研究基础,使赫胥黎成为细胞运动性领域的奠基人。