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Midterm 2 Actin uses.docx

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Western University
Biology 2382B
Robert Cumming

Conformational Changes of MyosiA nTP Driven myosin movement Skeletal Muscle Sarcomere along actin -in the absence of ATP, the myosin head is firmly attached to the actin filament. This state is very short lived in living muscle cells, it is the state responsible for muscle stiffness in death (rigor mortis) Step 1 On binding ATP, the myosin head releases from the actin filament Step 2 The head hydrolyzes the ATP -A Sarcomere is from one Z-Disk to the next to ADP and P, ihich induces a -The A Band contains thick myosin filaments; the I Band rotation in the head with respect to contains no myosin, just actin the neck. This states stores the -Sarcomere are repeating units -(-) end is inwards to myosin and (+) ends at Z Disk energy released by ATP hydrolysis -Myosin heads are (+) end direction; pull actin, shrink as elastic energy sarcomere -A Band doesn’t change size, I Band decreases; Z Disks Step 3 Myosin in the cocked state brought closer together binds actin Step 4 When it is bound to actin, the myosin head couples release of P i with release of the elastic energy to move the actin filament- known as the Power Stroke; as it involves moving the actin filament with respect to the end of the myosin neck domain Step 5 The head remains tightly -Sarcomere stable structure bound to the filament as ADP is Cap Z- bound to Z Disk Tropomodulin-capping (-) end released and before fresh ATP is bound by the head Nebulin- coating actin for stability Titin-Holding myosin in place; very elastic, compress and Sarcoplasmic Reticulum (SR) and Calcium Smooth Muscle Contractions (Myosin II) -Has high levels of Calcium (important in muscle contraction); Ca used as secondary messenger -Burst of Ca released from SR (surrounding sarcomere) -Transverse tubules; Invagination of PM interacts with SR through Ca release channel -Nerve impulse binds to PM; impulse=depolarization signal -Membrane charge hits Ca release channel, nerve impulse therefore releases Ca; quickly pumped back -Muscle slower contraction than skeletal muscle in to SR (Contraction); actively pumped back in -Digestive system/blood vessels -Myosin II can change shape due to phosphorylation; allows formation of thick filament -Regulation is slow via shape of myosin II; don’t want contraction then stop myosin from forming thick filament -Ca↑Phosphorylation of the myosin regulatory light -Ca binding to troponin/tropomyosin shifts their chain activates contraction; myosin can assemble into bipolar filaments to participate
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