Muscle Contraction and Cell Motility: Fundamentals and Developments

PrefaceI Skeletal Muscle Electron Microscopic Visualization and Recording of ATP-Induced Myosin Head Power Stroke Producing Muscle Contraction Using the Gas Environmental ChamberHistorical BackgroundMaterials and MethodsThe Gas Environmental ChamberCarbon Sealing Filmlontophoretic Application of ATPDetermination of the Critical Electron Dose Not to Impair Physiological Function of the SpecimenPosition-Marking of Myosin Heads with Site-Directed AntibodiesRecording of Specimen Image and Data AnalysisMyosin Head Movement Coupled with ATP Hydrolysis in Living Myosin Filaments in the Absence of Actin FilamentsStability in Position of Individual Myosin Heads in the Absence of ATPAmplitude of ATP-Induced Myosin Head Movement in Hydrated Myosin FilamentsReversal in Direction of ATP-Induced Myosin Head Movement across Myosin Filament Bare ZoneReversibility of ATP-Induced Myosin Head MovementAmplitude of ATP-Induced Movement at Various Regions within a Myosin HeadSummary of Novel Features of ATP-Induced Myosin Head Movement Revealed by Experiments Using the ECNovel Features of Myosin Head Power Stroke in the Presence of Actin FilamentsPreparation of Actin and Myosin Filament MixtureConditions to Record ATP-Induced Myosin Head Power Stroke in the Filament MixtureAmplitude of ATP-Induced Myosin Head Power Stroke in the Mixture of Actin and Myosin FilamentsReversibility of ATP-Induced Myosin Head Power StrokeSummary of Novel-Features of ATP-Induced Myosin Head Power Stroke Revealed by Experiments Using the ECAcknowledgmentReferencesStudies of Muscle Contraction Using X-Ray DiffractionIntroductionBasic Concepts in DiffractionEquatorial ReflectionsMeridional ReflectionsThe Full 2D Diffraction Pattern: Identifying Structural MechanismsConclusionAcknowledgementsReferencesMuscle Contraction Revised: Combining Contraction Models with Present Scientific Research EvidenceIntroductionFindings and Facts That Must Be Part of—or Explained by—a Model for ContractionStructure of the Contractile ApparatusGeneral structureProteins making up the contractile unitThe Internal Environment in a Muscle CellEnergy Consumption During ContractionATP consumption and ATPase rates during contractionElectric charge changes initiated by ATPActive Force DevelopmentStiffness and General Elastic Properties of the Contractile UnitThe Dynamic Contractile UnitWhat Happens during a Contraction?Importance of Considering Ion Movements as the Base for ContractionConclusionsAcknowledgementsReferencesLimitations of in vitro Motility Assay Systems in Studying Molecular Mechanism of Muscle Contraction as Revealed by the Effect of Antibodies to Myosin HeadIntroductionHistorical BackgroundDevelopment of in vitro Motility Assay SystemsIn vitro Force-Movement Assay SystemsProperties of Three Antibodies Used to Position-Mark Myosin Heads at Different Regions within a Myosin HeadDifferent Effects of three Antibodies to Myosin Head between in vitro Actin- Myosin Sliding and Muscle ContractionAntibody 1 (Anti-CAD Antibody) Has No Effect on Both in vitro Actin-Myosin Sliding and Muscle ContractionAntibody 2 (Anti-RLR Antibody) Inhibits in vitro Actin-Myosin Sliding, but Has No Appreciable Effect on Muscle ContractionAntibody 3 (Anti-LD Antibody) Shows No Marked Inhibitory Effect on in vitro Actin-Myosin Sliding, but Has Inhibitory Effect on Ca2+-Activated Muscle ContractionDefinite Differences in the Mechanism between in vitro Actin-Myosin Sliding and Muscle Contraction as Revealed by the Effect of Antibodies to Myosin HeadEvidence That Myosin Heads Do Not Pass through Rigor Configuration during Their Cyclic Attachment-Detachment with Actin FilamentsThe Finding That Anti-RLR Antibody Inhibits in vitro Actin-Myosin Sliding but Not Muscle Contraction Suggests That Myosin Head Flexibility at the Converter Domain Is Necessary for in vitro Actin-Myosin Sliding but Not for Muscle ContractionThe Finding That Anti-LD Antibody InhibitsConclusionReferencesCharacteristics and Mechanism(s) of Force Generation by Increase of Temperature in Active MuscleIntroductionMethods and MaterialsExperimental Techniques and ProceduresMuscle PreparationsAbbreviations, Nomenclature and Data AnalysesTemperature Dependence of Steady ForceIsometric Force and Force during Shortening/LengtheningEffects of Pi and ADP (Products of ATP Hydrolysis)Tension Response to Temperature-JumpDuring Muscle Shortening and LengtheningEffects of Pi and ADP on T-Jump Force GenerationA Minimal Crossbridge Cycle (and Modelling)Some General ObservationsUnresolved IssuesValue of Temperature-StudiesAcknowledgementsReferencesMechanism of Force Potentiation after Stretch in Intact Mammalian MuscleIntroductionMaterials and MethodsAnimals, Fibre Dissection and MeasurementsStatic Tension MeasurementsResultsStatic TensionEffects of Sarcomere Length on Active and Passive TensionEffects of Sarcomere Length on Static StiffnessDiscussionEquivalence between Residual Force Enhancement and Static TensionDependence of Static Stiffness on Sarcomere LengthBTS EffectsIndependence of Static Tension from CrossbridgesResidual Force Enhancement and Static Tension MechanismConclusionsGrantsReferencesThe Static Tension in Skeletal Muscles and Its Regulation by TitinIntroductionCharacteristics of the Static TensionMechanisms of Increase in Non-Cross-Bridge ForcesConclusion and Physiological ImplicationsAcknowledgementsReferencesStiffness of Contracting Human Muscle Measured with Supersonic Shear ImagingIntroductionMethods and MaterialsTheoretical Basis of Supersonic Shear ImagingSome Technical IssuesMuscle Activation Level and StiffnessAssociation of Shear Modulus with Joint TorqueAssociation of Shear Modulus with Motor Unit ActivityUsefulness as a Measure of Muscle Activation LevelRelations between Length, Force, and StiffnessLength-Dependent Changes in Shear ModulusLinear Association of Force and Shear ModulusDifference between Tetanic and Voluntary ContractionsStiffness Measured during Dynamic ContractionsDifferences in Shear Modulus among Contraction TypesPutative MechanismsGeneral Conclusions and PerspectivesAcknowledgmentsReferencesEffect of DTT on Force and Stiffness during Recovery from Fatigue in Mouse Muscle FibresIntroductionMethodsFibre Dissection and MeasurementsForce and Stiffness MeasurementsResultsDiscussionGrantsReferencesII CARDiAC and Smooth MuscleATP Utilization in Skeletal and Cardiac Muscle: Economy and EfficiencyIntroductionThe Crossbridge CycleDependence of ATP Utilization on Activity, Fiber Type and SpeciesATP Utilization in Cardiac MuscleThe Fenn EffectFuture PerspectivesReferencesEssential Myosin Light Chains Regulate Myosin Function and Muscle ContractionStructure and Interaction Interfaces of Essential Myosin Light ChainsStructure of Myosin IIStructure of Essential Myosin Light ChainsELC Interaction InterfacesELC PhosphorylationFunctional Roles of ELCs?ELC/MyHC InteractionsELC/lever arm interactionsELC/motor domain couplingsELC/Actin InteractionELC/RLC InteractionPhosphorylation of ELCFunctional Roles of ELC IsoformsStriated muscle ELC isoformsSmooth muscle ELC isoformsPathophysiology of ELCAcknowledgmentReferencesRegulation of Calcium Uptake into the Sarcoplasmic Reticulum in the HeartIntroductionSERCA2a Plays a Central Role in Ca2+UptakePhospholamban: A Critical Regulator of SERCA2aPLN Mutations Related to Human CardiomyopathyEnhancement of SR Function Is a Novel Therapeutic Target for Heart FailureStrategies to Increase SERCA2a Protein in Heart FailureStrategies to Modulate SERCA2a to Increase Ca2+ TransportStrategies to Decrease PLN Protein in Heart FailureStrategies to Disrupt the Interaction between SERCA2a and PLNSarcolipin, a Homologue of PLN, Is an Atrium-Specific Inhibitor of SERCA2aSarcalumenin Is a Newly IdentifiedConclusionReferencesThe Pivotal Role of Cholesterol and Membrane Lipid Rafts in the Ca2+- Sensitization of Vascular Smooth Muscle Contraction Leading to VasospasmIntroductionSPC Is a Causal Factor of Ca2+-Sensitization Leading to VasospasmThe Signaling Pathway of SPC-Induced Ca2+-Sensitization Leading to VasospasmRole of Cholesterol and Membrane Lipid Rafts in SPC-Induced Ca2+-Sensitization Leading to VasospasmSummaryAcknowledgmentsReferencesThe Catch State of Molluscan Smooth MuscleBackgroundStructures of Catch MusclesRegulation of CatchCatch TheoriesChallenges of the Traditional Myosin Head TheoryTwitchin BridgesMyosin Heads Tied by TwitchinMyorodInterconnections between Thick Filaments?Additional Kinases and PhosphatasesCatch during Active ContractionConclusionAcknowledgementsReferencesIII Cell Motility Regulation of Dynein Activity in Oscillatory Movement of Sperm FlagellaIntroductionBasic Features of Flagellar MovementDynein Force Generation and Microtubule Sliding in the AxonemeControl of Microtubule Sliding and Bend FormationRegulation of Dynein Activities by Mechanical SignalOutlookAcknowledgmentsReferencesThe Biomechanics of Cell MigrationIntroductionThe CytoskeletonCytoskeleton and Cell TypeFundamental Mechanism of Cell Migration Based on Actin Polymerization and Actomyosin ContractionThe Role of Microtubules in Maintaining Anterior-Posterior PolarityVariety of Cell Migration MechanismsTraction ForcesTraction Forces Exerted by FibroblastsTraction Forces Exerted by Dictyostelium Cells and NeutrophilsTraction Forces Applied by KeratocytesMechanosensing and Cell MigrationPassive MechanosensingActive MechanosensingContact GuidanceConclusion and Future PerspectivesAcknowledgementReferencesRole of Dynamic and Cooperative Conformational Changes in Actin FilamentsAn Exceptionally Conservative and Multifunctional Protein: ActinStructural Polymorphism of Actin FilamentsCooperative Conformational Changes of Actin Filaments Induced by ABPsInteraction with CofilinInteraction with MyosinInteraction with DrebrinInteractions with End-Binding ABPsPhysiological Roles of Cooperative Polymorphism of Actin FilamentsSegregation of ABPs along Actin FilamentsAmplification of the Inhibitory EffectIntracellular Signaling WireActin Filaments as MechanosensorsWhy Is Actin So Conservative?Possible Dynamic Roles of Actin Filaments in Muscle ContractionAcknowledgementReferences
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