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50.5: The physical interaction of protein
filaments Is required for muscle function
The types of effectors:Skeletal muscles .glands .smooth muscle
* Muscle contraction is the product of microfilament movement powered
by chemical energy.
Vertebrate Skeletal Muscle:
*They named skeletal because it is attach to a skeleton by a tendon.
*They consist of thousands of muscle fibers arranged longitudinally and
between them layers of connective tissue.
*They are striated, long, surrounded by plasma membrane (sarcolemma),
multinucleated (reflecting its formation by the fusion of many embryonic
cells).
*Each muscle consist of many microfibers
*The muscle fibers are arranged longitudinally, parallel to each other.
*Sacroplasm, nuclei, mitochondria, Sarcoplasmic reticulum are exist
between microfibrils.
*Each microfibril consists of microfilaments (myofilaments).
*The microfilaments are arranged in a special way that is repeated along
the myofibril we called sarcomere.
Refer to figure 50.26 page 1150
*The sarcomere is the basic, structural, contractile unit of the muscle.
*Each sarcomere is bordered by Z line (protein that anchors actin
filaments).
*In the middle of the sarcomere there are myosin filaments
*The region in the middle of the sarcomere is called M line (proteins that
anchor myosin filaments)
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Lecture 19
50.5: The physical interaction of protein
filaments Is required for muscle function
*At rest there is a partially overlapping between actin and myosin.. Near
the edge of the sarcomere there are only thin filaments, whereas the zone
in the center contains only thick filaments.
* A Band is a region of the myosin filaments length -- appear dark on
the microscope
*I Band Is a region between Z lines contain actin filaments -appear
light on the microscope
*H Band Is a region in the middle of the A Band -appear light on
the microscope
*The arrangement of the actin and myosin filaments is the key to how the
sarcomere contract and this regular arrangement of the filaments create a
pattern of light and dark bands (That is why we called it a striated
muscle)
Sliding-Filament model of muscle contraction
*The whole muscle, muscle fibers, myofibril, shortens when they contact,
but myofilaments (actin, myosin) they DON’T shorten instead they move
past each other increasing their overlap.
Refer to figure 50.27 page 1151
The structure of contractile filaments
Thin filaments (actin):
1. Two twisted strands of actin monomers (each is a globular
polypeptide)the filament is spherical
2. Two types of regulatory proteins :
 2 Tropomyosin strands coiled around the actin.(at rest it
covers the myosin-binding sites)
 Troponin complex bounded to the actin ,it consist of 3
subunits
 One binds to actin monomers
 One binds to Ca+2
 One binds to tropomyosin
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Lecture 19
50.5: The physical interaction of protein
filaments Is required for muscle function
At normal situations Ca+2 concentration is low in cytoplasm (It’s
congregate in the extracellular fluid or the sarcoplasmic reticulum)
*When Ca+2 bind to one Troponin subunit, a change in the conformation
of the Troponin occurs, this lead to movement of tropomyosin to expose
the myosin binding sites.
*At the relaxation of the muscle, the Ca+2 is removed from the
cytoplasm and returned to the extracellular fluid or the sarcoplasmic
reticulum, and the myosin binding sites are covered again by the
tropomyosin
Refer to figure50.29 Page 1152
Thick filaments(myosin):
*They are staggerd arrays of myosin molecules.
*Eeach myosin molecule consist of 2 polypeptide.(every polypeptide
has:)
1. Fibrous tail
2. Globular head(approximately 350 heads)
*The head is a motor protein that changes it’s conformation when it takes
energy (ATP)
* There is 2 region on the myosin head :1. A region that binds to the
myosin binding site on the actin filament to make a cross-bridge
2. A region that has ATPASE enzyme that hydrolysis ATP
Figure 50.28 page 1151
*The myosin-actin interaction need a lot of ATP
*ATP binds to head region then it’s hydrolyzed to ADP +inorganic
phosphate
* The energy released from ATP hydrolysis change the configuration of
myosin head from low to high energy configuration
*At the same time the myosin head binding site on the actin filament is
exposed by the presence of the Ca+2 .
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Lecture 19
50.5: The physical interaction of protein
filaments Is required for muscle function
*When the cross-bridge is formed, ADP +inorganic phosphate is released
and myosin head return to the low energy configuration, so it pulls the
actin to the middle of the sarcomere.
* To break the cross- bridge we need ATP, then ATP binds to the myosin
head and the cycle is repeated.
* The skeletal muscles don’t contract unless they’re stimulated by a
motor neuron remember the skeletal muscle is an excitable cell which
means we can convert the electrical current in it to an action.
*The 350 heads of the thick filament forms and re-forms about 5 crossbridges per second
* The ATP that already exists is enough or only few contractions….To
power repetitive contractions the muscle cell relies on 2 other storage
compounds:
1. Creatine phosphate(Formed in the liver and pancreas)  Transfer
of phosphate group from creatine phosphate to ADP(an endergonic
reaction) in an enzyme-catalyzed reaction synthesizes additional
ATP- it can sustain contraction for 15 seconds
*The hydrolysis of excess creatine produces Creatinine which is
used for the kidney function test.
2. Glycologen The broken of glycologen to glycose generates ATP
by either (aerobic respirationcan sustain contraction for nearly an
hour) or by ( glycolosis  it can sustain contraction for 1 minute )
The role of calcium and regulatory proteins
Figure50.30page1153
*Each microfibril is surrounded by a sarcoplasmic reticulum
* When action potential arrives to the synaptic terminals of a motor
neuron, the acytelcholin (neurotransmitter) is released, and then it binds
to the ligand gated ion channel on the muscle fiber leading to a
depolarization.
*The action potential spreads along the plasma membrane and down the
Transfer (T) tubule ( infolding from the plasma membrane filled
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Lecture 19
50.5: The physical interaction of protein
filaments Is required for muscle function
with the interstitial fluid and they’re located in specific sites in each
skeletal muscle cell)
* T tubule makes a close contact with sarcoplasmic reticulum SR
*The action potential triggers Ca+2 release from SR by opening the Ca+2
channels in the membrane of the SR
*Ca+2 bind to the Troponin complex, initiating contraction of the muscle
fibers
* When motor neuron input stops, the muscle cells relaxes
 Filaments slide back to their starting position
 Cytosolic Ca+2 is removed by Active transport using Ca+2 pump
into SR.
*some diseases cause paralysis by interfering with the excitation of the
skeletal muscles by the motor neuron (at the neuromuscular junction):
1. amyotrophic lateral sclerosis ALS (also called Lou Gehrig’s disease):
the motor neurons in the spinal cord and brainstem degenerate, and the
muscle fibers with which they synapse atrophy. It’s progressive and
fatal in 5 years after the symptoms appear  no cure or treatment.
2. Myasthenia gravis (A type of autoimmune disease): a person produces
antibodies to the acetylcholine receptors on skeletal muscle fibers, as the
number of these receptors decreases, synaptic transmission between
motor neurons and muscle fibers declines  there are effective
treatments.
3. Botulism: which is typically fatal because muscles required for
breathing fail to contract when acetylcholine release is blocked  also
used in cosmetic procedures as BOTOX.
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Lecture 19