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Identifying Mechanisms of Thin Filament Activation in Cardiac Muscle Contraction: the Effects of Myosin Cross-Bridges John L

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Identifying Mechanisms of Thin Filament Activation in Cardiac Muscle Contraction: the Effects of Myosin Cross-Bridges John L Florida State University Libraries Electronic Theses, Treatises and Dissertations The Graduate School 2012 Identifying Mechanisms of Thin Filament Activation in Cardiac Muscle Contraction: The Effects of Myosin Cross-Bridges John L. Williams Follow this and additional works at the FSU Digital Library. For more information, please contact [email protected] THE FLORIDA STATE UNIVERSITY COLLEGE OF ARTS AND SCIENCES IDENTIFYING MECHANISMS OF THIN FILAMENT ACTIVATION IN CARDIAC MUSCLE CONTRACTION: THE EFFECTS OF MYOSIN CROSS-BRIDGES By JOHN WILLIAMS A dissertation submitted to the Department of Biological Science in partial fulfillment of the requirements for the degree of Doctor of Philosophy Degree Awarded: Fall Semester, 2012 John Williams defended this dissertation on September 12th, 2012. The members of the supervisory committee are: P. Bryant Chase Professor Directing Dissertation Michael Overton University Representative W. Ross Ellington Committee Member Thomas Keller Committee Member Piotr Fajer Committee Member The Graduate School has verified and approved the above-named committee members, and certifies that the dissertation has been approved in accordance with university requirements. ii I dedicate this dissertation to the memory of my late grandmothers, Lucille Williams and Thelma Davis, who from an early age became my inspirations for pursuing a career in science. I dedicate this to my parents who have been instrumental in my development both academically and socially, and who made every effort during my childhood years to make sure that I received the love and support needed to be successful as I progressed during this educational journey. I dedicate this to my mentors at Albany State University and at Florida State University who saw something in me worth supporting, even when I was in personal doubt of my abilities and capabilities. And lastly, I dedicate this to the young men and women in my family and my community for whom I have served as a mentor, as a testament that education can take you further in life than your dreams could ever imagine. While this was an arduous task, and is only one of many milestones to come in my lifetime, I recognize that without the advent of these God- given people in my life, I would not have made it this far, and for them I am appreciative and grateful. iii ACKNOWLEDGEMENTS I would like to acknowledge the contributions made by many different parties during the course of this dissertation research. I would like to thank the committee of Drs. Chase, Overton, Ellington, Fajer, and Keller for continued support and providing challenging and thought- provoking critique that helped me to define the goals and procedures of my work. Additionally, I would like to thank Dr. Bryant Chase for providing mentorship and tutelage that has assisted me in understanding the nature of muscle biology and, specifically, cardiac muscle physiology. I would like to thank the Chase Laboratory members, past and present, for providing technical assistance whenever possible, which proved to be priceless throughout my matriculation. I also want to thank the Department of Biological Science here at Florida State University for providing the financial and professional support needed to assist in this process. From a personal standpoint, I would like to thank my family and friends for providing the moral support that was critical for the completion of my dissertation work. My parents, who have always been willing to assist whenever possible, have been instrumental in my daily battles with errant data, difficult tasks, and life issues. My friends and colleagues at FSU have provided excellent peer-to-peer support that essentially made my time here much smoother. And lastly, and most importantly, I would like to thank God for providing me the strength to stay the course through this journey and to keep pushing when quitting was an option. iv TABLE OF CONTENTS List of Abbreviations vii List of Tables viii List of Figures ix Abstract x 1. INTRODUCTION 1 Cardiac Muscle Tissue 2 Excitation-Contraction Coupling 7 Cross-bridge Cycling 8 Cooperativity in Striated Muscle 12 2. PROTEIN ISOLATION: METHODS AND SOURCES 21 Extraction of Porcine Cardiac Myosin 21 Potassium-EDTA ATPase Assay 22 Myosin Proteolysis and Isolation of Porcine Cardiac Heavy Meromyosin 24 Isolation of Filamentous (F) Actin 25 Isolation of Human Cardiac Troponin and Tropomyosin 25 New Protocol for Isolation of Porcine Cardiac Heavy Meromyosin 26 3. INVESTIGATING COOPERATIVITY USING IN VITRO MOTILITY ASSAYS 29 In Vitro Motility Using Cardiac Muscle Proteins 29 AIM I: Establishing the Conditions for Conducting Motility Assays Using Unregulated Actin Filaments 34 The Effects of Temperature on Motility of Unregulated F-Actin 34 The Effects of pcHMM Surface Density on Unregulated F-Actin Sliding Speeds 35 AIM II: Investigating the Effects of Myosin Cross-bridges on Thin Filament Activation 37 The Effects of pcHMM Surface Density on Ca2+- Dependent Sliding Speed of Reconstituted Thin Filaments 37 v Influence of Filament Length on Sliding Speed of Unregulated F-actin and Regulated Thin Filaments 39 4. DISCUSSION OF RESULTS: NEW INSIGHTS INTO THE MECHANISMS OF CARDIAC THIN FILAMENT ACTIVATION 45 The Effects of Cross-bridge Number on In Vitro Motility Assays with Unregulated F-Actin 45 Cardiac HMM versus Skeletal HMM Surface Densities: Comparison with Previous Literature 49 Filament Length Dependence of Sliding Speed: F-actin versus Regulated Thin Filaments at pCa 5 52 Filament Length Dependence of Sliding Speeds: Reconstituted Thin Filaments at pCa 5 and pCa 7 53 Cooperative Activation of the Thin Filament by Ca2+ 58 Limitations of the Study 60 5. CONCLUSIONS AND DIRECTION FOR FUTURE STUDY 64 Implications 66 6. APPENDICES 71 A. Buffers for HMM Preparation 71 B. Buffers for Myosin Extraction 72 C. Isoform Differences and Chemical Properties of Rodent and Porcine Myosins 74 7. REFERENCES 75 8. BIOGRAPHICAL SKETCH 82 vi LIST OF ABBREVIATIONS AFM -Atomic force microscopy ATP -Adenosine triphosphate ATPase -ATP hydrolysis Ca2+ -Calcium (divalent cation) CICR- Calcium induced calcium release ddH2O-Double-deionized water DTT- dithiothreitol EC - Excitation-contraction coupling F-actin- Filamentous actin FHC- Familial hypertrophic cardiomyopathy IPTG- Isopropyl β-D-1-thiogalactopyranoside IVM-In vitro motility kD-Kilo Dalton MHC Myosin heavy chain n- Hill coefficient PBS- Phosphate buffered saline pCa -Negative log (base 10) of ion concentration, where [Ca2+] is in molar pCa50 -The pCa at which force or sliding speed at which 50% of maximum value is attained pcMyosin -Porcine cardiac myosin pcHMM- Porcine cardiac heavy meromyosin Pi- Inorganic phosphate rhcTm -Recombinant human cardiac tropomyosin rhcTn -Recombinant human cardiac troponin RhPh- Rhodamine phalloidin rsMyosin -Rabbit skeletal myosin SR- Sarcoplasmic reticulum Tm- Tropomyosin Tn- Troponin vii LIST OF TABLES TABLE 1: Cooperativity as Defined by Functional and Structural Regulatory Units 20 TABLE 2: Decreasing Temperatures Leads to Active pcHMM Fragments 27 viii LIST OF FIGURES 1-1 Histology of Cardiac and Skeletal Muscle 4 1-2 Myosin II 5 1-3 Calcium Induced Calcium Release in the Heart 11 1-4 Myosin Heads Form Cross-bridges with Actin Monomers on the Thin Filament 11 2-1 Atomic Force Microscopy Image of Myosin Molecules after Extraction 23 2-2 Isolated Porcine Cardiac Myosin Retains ATPase Activity 23 2-3 Isolation of PcHMM 27 2-4 Structure of Myosin II Preparations 28 3-1 Schematic of the In Vitro Motility Flow Cell 32 3-2 Schematic of the In Vitro Motility Assay 32 3-3 Tracking of Individual Filaments and Analysis of Filament Sliding Speeds 33 3-4 Increasing Temperature of Motility Increases Filament Sliding Speeds 36 3-5 Increasing [pcHMM] Generally Increases Sliding Speed of Unregulated F-actin 36 3-6 Speed-pCa Curves for Regulated Thin Filaments at 100 and 200 g/ml pcHMM Applied to the Flow Cell Surface. 41 3-7 Sliding Speed for Regulated Thin Filaments at pCa 5 Increases Relative to the Speed of Unregulated F-actin as Surface Density Increases 42 3-8 Sliding Speed Varies with Filament Length at 150 g/ml [pcHMM] Applied 43 3-9 Sliding Speed Varies with Filament Length at 200 g/ml [pcHMM] Applied 43 3-10 Reconstituted Thin Filament Sliding Speed is More Affected by Cross-bridge Number (Density) at pCa 5 than at pCa 7 44 ix 5-1 A Schematic of Thin Filament Activation 69 5-2 A Simple Positive Feedback Mechanism of Ca2+-based Activation of the Thin Filament 70 x ABSTRACT Myocardial contractions are generated by the binding of myosin motor proteins to cardiac actin in the thin filament. This process is regulated by the binding of calcium ions to troponin C. When Ca2+ binds to site II of troponin C, the troponin complex undergoes a conformational change which displaces tropomyosin and uncovers the myosin-binding sites on actin. This allows myosin to bind, and in the presence of ATP, allows for cross-bridges to cycle in order to generate force. While calcium binding to troponin is considered to be the key regulating mechanism for striated muscle contraction, myosin cross-bridges are also thought to play a role in cooperatively activating the thin filament. This cross-bridge contribution to thin filament activation appears to be more important in cardiac muscle systems than it is in skeletal muscle. However, many of these experiments examined the effects of cross-bridges under non- physiological conditions, leading to questions about the importance of actively cycling cross- bridges. Furthermore, there are questions as to the contribution of cross-bridge activation under conditions of low cross-bridge number, such as during filament sliding, primarily due to the inability to effectively change the number of cross-bridges that bind within a system in a controlled manner. In order to examine this possibility, I developed a porcine cardiac heavy meromyosin fragment that could be used to effectively vary the amount of myosin cross-bridges present in the in vitro motility assay.
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