Skeletal Muscle Contraction Sliding Filament Model actin myosin Fig. 11.3.
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Transcript of Skeletal Muscle Contraction Sliding Filament Model actin myosin Fig. 11.3.
![Page 1: Skeletal Muscle Contraction Sliding Filament Model actin myosin Fig. 11.3.](https://reader036.fdocuments.us/reader036/viewer/2022062300/56649cbf5503460f94985186/html5/thumbnails/1.jpg)
Skeletal Muscle ContractionSliding Filament Model
actinmyosin
Fig. 11.3
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Thin (actin) filament
actin monomerG-actin(globular actin)
actin polymerF-actin(filamentous actin)
from Alberts et al.,Molecular Biology of the Cell
Fig. 11.3
Fig. 3-3 Ganong
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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 zonecentral bare zone
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Striated Muscle
A- band(anisotropic)contains thick filaments(and portions of thin filaments)
I- band(isotropic)contains thin filaments
Fig. 3-2Ganong
Fig. 3-3 Ganong
Fig. 11.1
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Striated MuscleFig. 11.4
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Striated Muscle
Fig. 11.2
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Sliding Filament Model of Contraction
Fig. 3.3 Ganong
Fig. 11.9
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Cross Bridge Cycle
Fig. 11.9
As myosin heads bind ATP, the crossbridges detach from actin, become reoriented and hydrolyze ATP to ADP and Pi.
No ATP no detachmente.g., rigor mortis
The myosin head isan ATPase.
The two most important shape-changing events are13/10 ATP binding (which
leads to detachment and reorientation)
11/12 Pi release (which leads to the power stroke)
causes Pi to be released.
Power stroke causes ADP to be released
Pi
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ATP binding to myosin
Fig. 3-6 Ganong (19th edition)
The image above and the modifications to the Saladin text in the previous slideare 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, 4th ed., 2002)
ATP binding is more important for reorientation than ATP hydrolysis.
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Length-Tension Relationship
Increased muscle length causes decreased overlapbetween thick andthin filaments.
Increased muscle diameter causes increased separation(the lattice spacing)between thick andthin filaments.(actual mechanism still a topic of debate, see Fuchs and Martyn, Length-dependent Ca2+ activation in cardiac muscle: some remaining questions. J. Muscle Res. and Cell Motility, 26:199-212, 2005)
= normal operating length for skeletal muscle
= normal operatinglength for cardiacmuscle
Fig. 11.11
ly short