WorldCat Identities

Spudich, James A.

Overview
Works: 36 works in 54 publications in 1 language and 504 library holdings
Genres: Conference proceedings  Periodicals 
Roles: Editor, Author, Thesis advisor
Classifications: QH585, 574.87
Publication Timeline
.
Most widely held works by James A Spudich
Dictyostelium discoideum : molecular approaches to cell biology by James A Spudich( Book )

11 editions published in 1987 in English and held by 225 WorldCat member libraries worldwide

Molecular genetic approaches to protein structure and function : applications to cell and developmental biology( Book )

4 editions published in 1989 in English and held by 113 WorldCat member libraries worldwide

The cytoskeleton( Book )

1 edition published in 1996 in English and held by 30 WorldCat member libraries worldwide

Annual review of cell biology and developmental biology( Book )

2 editions published in 1996 in English and held by 12 WorldCat member libraries worldwide

Annual review of cell developmental biology( Book )

1 edition published in 1998 in English and held by 12 WorldCat member libraries worldwide

Annual review of cell biology and developmental biology( Book )

1 edition published in 1995 in English and held by 9 WorldCat member libraries worldwide

Methods in cell biology / molecular approaches to cell biology / edited by James A. Spudich( Book )

2 editions published in 1987 in English and held by 4 WorldCat member libraries worldwide

Single myosin molecule mechanics a lecture( Visual )

1 edition published in 1995 in English and held by 2 WorldCat member libraries worldwide

Annual review of cell biology( Book )

1 edition published in 1995 in English and held by 2 WorldCat member libraries worldwide

Annual review of cell biology( Book )

1 edition published in 1997 in English and held by 2 WorldCat member libraries worldwide

Annual review of cell biology( Book )

1 edition published in 1996 in English and held by 2 WorldCat member libraries worldwide

Annual review of cell biology( Book )

1 edition published in 1988 in English and held by 2 WorldCat member libraries worldwide

The nature and origin of bacterial spore proteins by James A Spudich( )

2 editions published in 1967 in English and held by 2 WorldCat member libraries worldwide

Annual review of cell and developmental biology by James A Spudich( Book )

2 editions published between 1995 and 1998 in English and held by 2 WorldCat member libraries worldwide

Advanced single molecule fluorescence analysis and force spectroscopy to understand myosin motors by Jongmin Sung( )

1 edition published in 2013 in English and held by 1 WorldCat member library worldwide

Myosins are actin-based molecular motor proteins that are associated with numerous cellular functions both in muscle and non-muscle cells. In the past decades, single molecule biophysics has provided many useful in-vitro techniques that enable one to understand detailed molecular mechanisms of myosin-actin interaction. I will describe our results and continuing efforts in (i) single-molecule fluorescence localization analysis with TIRF microscopy, and (ii) single-molecule force spectroscopy with optical traps to understand myosin motors. Our theoretical point-spread function combined with maximum-likelihood-estimation precisely extracts both positions and orientations of fixed fluorescent molecules simultaneously. This approach is now mature as a structural tool, and I have applied it to two examples: myosin V labeled with a fixed dye walking on actin filaments, and dsDNA with two differently colored probes doubly attached to its backbone. We experimentally show that our method is not only precise but also accurate. Familial hypertrophic cardiomyopathies (HCM) are common genetic heart diseases that are often caused by single point mutations, especially in human beta cardiac myosin II. Using an optical trap assay, we found that the human beta cardiac myosin with the R453C HCM-causing mutation produces significantly elevated intrinsic force. We further developed a new method called harmonic force spectroscopy that can extract a force-velocity curve from a single cardiac myosin molecule. We found that a strong-to-weak transition of a cardiac myosin bound to an actin filament is modulated by an external load, which can be explained by simple Arrhenius transition theory
Understanding the molecular mechanisms of cardiomyopathy-causing mutations in sarcomeric proteins by Ruth Sommese( )

1 edition published in 2013 in English and held by 1 WorldCat member library worldwide

Heart disease is one of the leading causes of morbidity and mortality in the developed world. As such, significant amount of resources and energy are funneled into developing treatments and therapeutics. While genetically caused cardiovascular diseases manifest at the tissue level, the fundamental mechanism that triggers the secondary effects and tissue remodeling generally occurs at the protein level. It is therefore critical to understand the molecular changes on the basic biochemical and biophysical level and connect these to the cellular and developmental disease processes. One such cardiovascular disorder is hypertrophic cardiomyopathy or HCM, which has been estimated to affect approximately 1 in 500 individuals. It disproportionately affects young adults and is the leading cause of sudden cardiac death. Since the first case of genetically linked HCM was identified in the early 1990s, a significant amount of work has been done to understand the molecular mechanism of the disease. Mutations have been identified in the proteins comprising the contractile apparatus of the muscle, the sarcomere. One such protein is [beta]-cardiac myosin, which has been recognized as a significant culprit of genetically linked HCM (~30-50%). Many studies have been performed to understand how single point mutations can alter the enzymatic and mechanical properties of this motor protein, but there is no clear consensus about the molecular mechanism. This has been due mainly to the lack of available human [beta]-cardiac myosin and the use of non-human and non-[beta]-cardiac myosin. Non-human and non-[beta]-cardiac myosin from common animal models differ by >30 residues, and as clearly evident from the disease and from previous studies on myosin, a single amino acids mutation can significantly alter and disrupt myosin function. During my thesis work, I have performed the first biochemical and biophysical work in the field looking at cardiomyopathy mutations using human [beta]-cardiac myosin. I have shown that HCM-causing [beta]-cardiac myosin mutations result in a gain of function, increasing the power or work output of the myosin. I have also examined HCM-causing mutations in troponin T, a component of the thin filament regulatory unit, using human [beta]-cardiac myosin. In the muscle, the interaction of myosin and actin is regulated by calcium through the thin filament proteins, namely the troponin complex and tropomyosin. HCM-causing mutations in troponin T increase calcium sensitivity or the number of force-producing heads that can interact with actin, thereby also increasing force or power output in the muscle. My work not only sheds light on fundamental properties of thick and thin filament function in the human sarcomere and presents the first studies of HCM-causing mutants in a human background, it also establishes a new approach to the problem of cardiomyopathy that will be critical in truly understanding and targeting the disease
Probing mechanisms of myosin motors using single molecule techniques by Mary Williard Elting( )

1 edition published in 2012 in English and held by 1 WorldCat member library worldwide

Members of the myosin family of molecular motors perform a variety of essential functions in the cell, including powering muscle contraction and cell division, transporting cargo, and serving as anchors and tension generators. Myosins accomplish these tasks by transforming chemical energy from ATP hydrolysis into mechanical work, as they either move along their actin filament tracks, or power the movement of the actin filaments. Single molecule techniques have proven especially useful for understanding the biophysical mechanisms that myosins employ in order to perform their functions. In this thesis, I discuss my application of quantitative, single molecule level approaches to remaining questions about the mechanisms of myosins II, V and VI. In the first section, I describe our analysis of myosin VI processivity via structurally engineered mutant constructs, which we examined using single molecule fluorescence. Myosin VI is both structurally and functionally unusual among myosins. In order to probe our understanding of its mechanism, we replaced its lever arm with a variety of engineered artificial lever arms, and tested whether it responded as we would expect. As part of this work, I also developed a quantitative model of processivity of myosin VI, which I used to analyze the expected effects of decreasing intramolecular communication between the heads of a processive myosin. This model has implications not only for myosin VI, but for other two headed processive motors, including processive myosins, kinesins, and dyneins. In this work, I found that processivity is markedly robust to decreased inter-head communication. In order to further characterize intramolecular communication in processive myosins V and VI, I hoped to directly visualize ATP molecules binding and releasing from myosin molecules as they walked along actin filaments. This required the development of techniques to allow the resolution of single fluorescent molecules at higher concentrations of fluorophore than has previously been possible. I approached this challenge using two technological approaches: linear zero mode waveguides (ZMW) and convex lens induced confinement (CLIC). While the direct visualization of nucleotide gating remains a challenge, I made significant progress toward applying these techniques to that outstanding question. Finally, in the last section of my thesis, I discuss work on characterizing mutations in the human cardiac myosin II protein that cause hypertrophic and dilated cardiomyopathy. While many mutations that cause these diseases have been identified, their mechanism(s) of action are not understood. Characterizing these effects requires precise quantification, since the changes in myosin behavior caused by the mutations are likely to be subtle. Toward that end, I have refined our approach to the gliding filament assay to increase its precision and reproducibility, and have begun to characterize the effects of several disease-causing mutations in this motor
Spatiotemporal dynamics from interlinked positive-and-negative feedback loops by Tony Yu-Chen Tsai( )

1 edition published in 2013 in English and held by 1 WorldCat member library worldwide

Positive and negative feedback loops are two of the most ubiquitous network motifs in biological systems. When a positive feedback loop and a negative feedback loop are coupled together, rich dynamics can emerge. Among these, oscillations in time and space, and pulses of protein activity are some of the commonly observed phenomena in a biological system. In this thesis, we started by computationally study the benefit of a positive feedback in an oscillator, and concluded that oscillators running on interlinked positive-and-negative feedback loops are more robust and tunable in period than the oscillators with only the negative feedback. We then focused on the Xenopus laevis embryonic cell cycle oscillator, a well characterized biochemical oscillator that runs on interlinked positive-and-negative feedback loops. We identified a transition of oscillator topology during Xenopus early development, from the long first cell cycle that depends critically on Wee1/Cdc25 mediated positive feedback, to the short subsequent cell cycles in which the positive feedback is dispensable. Using the human neutrophil-like HL60 cells, we studied the spatiotemporal dynamics of cytoskeleton proteins. We identified a perfect coupling between the protruding front and the retracting rear of a migrating HL60 cells. Myosin exhibits dynamic flashes at the rear of the cell, and the time scale of the flashes depends on local positive and negative feedback loops. When the duration of the myosin flashes is perturbed, the cell exhibits difficulties in turning and has inefficient chemotaxis. We also performed a statistical study comparing the shape and migration dynamics of HL60 cells, and provided evidence of a close correlation between the two phenotypes. Our results showed that the spatiotemporal protein dynamics allowed by proper regulation of interlinked positive-and-negative feedback loops is important in many examples in biology
Dictyostelium discoideum Molecular Approaches to Cell Biology. Methods in Cell Biology, Volume 28( )

2 editions published in 1987 in English and held by 0 WorldCat member libraries worldwide

METHODS IN CELL BIOLOGY,VOLUME 28: DICTYOSTELIUM DISCOIDEUM: MOLECULAR APPROACHES TO CELL BIOLOGY
Methods in Cell Biology, 28 by James A Spudich( )

1 edition published in 1987 in English and held by 0 WorldCat member libraries worldwide

METHODS IN CELL BIOLOGY, VOLUME 28: DICTYOSTELIUM DISCOIDEUM: MOLECULAR APPROACHES TO CELL BIOLOGY
 
moreShow More Titles
fewerShow Fewer Titles
Audience Level
0
Audience Level
1
  Kids General Special  
Audience level: 0.63 (from 0.58 for Annual rev ... to 0.88 for The nature ...)

Alternative Names
James A. Spudich US-amerikanischer Biochemiker

James Spudich biochimico statunitense

詹姆斯·斯普迪赫

Languages
English (38)

Covers
The cytoskeletonAnnual review of cell biology and developmental biologyAnnual review of cell developmental biologyAnnual review of cell biologyAnnual review of cell biologyAnnual review of cell and developmental biologyMethods in Cell Biology, 28