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Skeletal Muscle Contraction Sliding Filament Model actin myosin Fig. 11.3.

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Presentation on theme: "Skeletal Muscle Contraction Sliding Filament Model actin myosin Fig. 11.3."— Presentation transcript:

1 Skeletal Muscle Contraction Sliding Filament Model actin myosin Fig. 11.3

2 Thin (actin) filament actin monomer G-actin (globular actin) actin polymer F-actin (filamentous actin) from Alberts et al., Molecular Biology of the Cell Fig. 11.3 Fig. 3-3 Ganong      

3 Thick (myosin) filament myosin molecule (“monomer”): 2 heavy chains + 4 light chains Fig. 11.3 from Alberts et al., Molecular Biology of the Cell central bare zone

4 Striated Muscle A- band (anisotropic) contains thick filaments (and portions of thin filaments) I- band (isotropic) contains thin filaments Fig. 3-2 Ganong Fig. 3-3 Ganong Fig. 11.1

5 Striated Muscle Fig. 11.4

6 Striated Muscle Fig. 11.2

7 Sliding Filament Model of Contraction Fig. 3.3 Ganong Fig. 11.9

8 Cross Bridge Cycle Fig. 11.9 As myosin heads bind ATP, the crossbridges detach from actin, become reoriented and hydrolyze ATP to ADP and P i. No ATP  no detachment e.g., rigor mortis The myosin head is an ATPase. The two most important shape-changing events are 13/10 ATP binding (which leads to detachment and reorientation) 11/12 P i release (which leads to the power stroke) causes P i to be released. Power stroke causes ADP to be released PiPi

9 ATP binding to myosin Fig. 3-6 Ganong (19 th edition) The image above and the modifications to the Saladin text in the previous slide are based on Raiment et al., Science 261:50-58, 1993, and Vale and Milligan, Science 288:88-95, 2000. (see also Fig. 16.58 in Alberts et al., Molecular Biology of the Cell, 4 th ed., 2002) ATP binding is more important for reorientation than ATP hydrolysis. 

10 Length-Tension Relationship Increased muscle length causes decreased overlap between thick and thin filaments. Increased muscle diameter causes increased separation (the lattice spacing) between thick and thin filaments. (actual mechanism still a topic of debate, see Fuchs and Martyn, Length- dependent Ca 2 + activation in cardiac muscle: some remaining questions. J. Muscle Res. and Cell Motility, 26:199-212, 2005) = normal operating length for skeletal muscle = normal operating length for cardiac muscle Fig. 11.11 ly short


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