Lecture 20 (11b) - Cell Communication Part 2 Flashcards
Record jumps
Frog - Rosie (6.5m)
Human - Jackie Joyner Kersee (7.m)
three types of vertebrate muscle
- skeletal
- cardiac
- smooth
Skeletal muscle
- voluntary movement, breathing, maintaining posture
* appear striped bc of regular arrangement of sarcomeres
Cardiac muscle
- beating of heart
* cells interdigitate, forming a mesh
Smooth muscle
- involuntary, movement of internal organs
* do NO have stripes of regularly arranged actin and myosin
One muscle is composed of
hundreds of thousands of muscle cells (fibers) bundle together with connective tissue
One cell is called a
muscle fiber - large and multinucleate
• comes from the fusion of many myoblasts during development)
Each muscle cell (one fiber) consists of
several myofibrils
1 muscle fiber = 1 cell
actin + myosin --> sarcomere --> myofibril --> muscle fiber + CT --> 1 muscle
Muscle cells need lots of
mitochondria to make ATP
Muscle cell membrane
sarcolema
Muscle cell cytoplasm
sarcoplasm
Each myofibril consists of repeating units called
sarcomeres
Each sarcomere is made of
overlapping actin and myosin filaments
1 sarcomere is from
Z line to Z line
I band
actin
A band
myosin with overlapping actin
• darker because myosin is thinner
H zone
only myosin
Each myofibril =
plenty of sarcomeres repeating horizontally
Each sarcomere is bound by
Z lines which anchor the actin
A band
in the middle of the sarcomere
• all the myosin filaments
H zone
non overlapping part of actin
I band
non overlapping part of myosin
H zone and I band
non overlapping part of actin and myosin
Titin
holds the myosin to the Z
• “bungee cord” = resistance to stretch in a relaxed muscle
Sliding filaments cause the muscle to contract
actin slides past myosin = contraction
When a muscle contracts
- sarcomeres shorten and band pattern changes
* non overlapping parts - H and I - diminish because there is more overlapping between actin and myosin filaments
2 main actors of the muscle contraction
myosin and actin
Myosin
2 polypeptide chains coiled together, ending in a globular head
• a myosin filament is made of many molecules in parallel with heads projecting sideways
Actin filament
actin monomers in a long twisted molecule
Tropomyosin is twisted around
actin
• troponin binds to tropomyosin, which binds to actin
Troponin has 3 subunits and each of them binds to
- tropomyosin
- actin
- Ca2+
Calcium binds to
troponin • 1 site changes conformation and changes conformation of tropomyosin and twist tropomyosin around actin --> reveals hidden site --> binds to myosin
Actin and myosin can interact
there is a binding site on actin for myosin
BUT ONLY WHEN THERE IS CA2+
By default, the actin sites for myosin
are hidden,
but when there is Ca2+ in the sarcoplasm,
it binds to troponin,
troponin changes conformation,
which twists the tropomyosin around the actin to
expose actin sites for myosin
• myosin head binds –>
changes conformation, head bends
= actin moves relative to myosin
(5-10nm)
The role of the Ca2+
- when actin sites are exposed, the myosin head can bind the specific sites on actin to form cross-bridges between myosin and actin
- when myosin head binds the actin, the head conformation changes, the head bends and causes a tiny force that causes the actin filament to move 5-10 nm relative to the myosin filament
The role of ATP
- when a myosin head is bound to actin, it can bind a hydrolyze ATP
- the energy released when it binds ATP changes the conformation of the head again and causes it to release the actin and return to its extended position
- the head is now ready to start a new binding with actin (new cycle)
- ATP contributes to myosin and actin dissociation
myosin head bound, binds and hydrolyzes ATP, changes head conformation –> releases actin
Rigor mortis (right after death)
- ATP production stops, and so myosin can’t release actin filaments and muscles stay contracted
- eventually the proteins lose their integrity and the muscles soften
- timing of these events help medical examiners examine the time of death
Repetition of a cycle
- contraction of the sarcomere involves many consecutive cycles of interaction between actin and myosin molecules
- when a cycle is over, a single myosin head breaks its contact with actin
- the actin filaments do not slip backward because there are many other myosin heads attached to the actin filament
- as long as Ca2+ and ATP are available, the cycle of actin and myosin interactions continues and the filaments slide past each other
1 binds, another releases
• actin doesn’t slip back bc myosin is still grabbing
End of the contraction
- when Ca2+ pumps (active pumps requiring ATP) remove Ca2+ from sarcoplasm, contraction stops…
- when absence of Ca2+, tropomyosin twists back to its original conformation and is hiding the actin site for myosin
- Ca2+ always pumped inside
- need Ca2+
(usually low concentration in sarcoplasm bc of Ca pump)
The sliding of actin and myosin is regulated by
the sarcoplasmic concentration of calcium ions
Muscle cells are
excitable - the plasma membrane can conduct action potentials
Contraction is initiated by
action potentials from a motor neuron at the neuromuscular junction
Motor unit
one motor neuron and all the muscle fibers it synapses with (3-1,000)
The neuromuscular junction
the fibers in a motor unit contract simultaneously when the neuron fires
Chemical synaptic transmission begins with
the arrival of an action potential
The action potentials in muscle fiber travel
deep within the cell
The plasma membrane is continuous with
T tubules that run through the sarcoplasm
T tubules run close to the
sarcoplasmic reticulum (muscle fiber ER) that surrounds every myofibril
T tubule
fold (in) of sarcolema around myofibril
• action potential through membrane, depolarize through T tubule
• meets sarcoplasmic reticulum that’s full of Ca2+
The sarcoplasmic reticulum is full of
Ca2+
The T tubule is connected to the sarcoplasmic reticulum by
receptor proteins
Channel opens in sarcoplasmic reticulum with action potential –>
Ca2+ into sarcoplasm and available for myofibrin
Ca2+ binds to
tropomyosin
In the resting muscle, the Ca2+ is highly concentrated in
the sarcoplasmic reticulum
Ca2+ has a low concentration in the sarcoplasm thanks to
the active pumps of Ca2+ in the sarcoplasmic reticulum membrane that pumps it back from the cytoplasm to the sarcoplasmic reticulum
An action potential spreads through the T tubules…
when it reaches the receptor proteins, they change conformation
• this opens Ca2+ channels and
Ca2+ flows out of the sarcoplasmic reticulum
Summary of contraction
- release of Ca2+ from the sarcoplasmic reticulum triggers muscle contraction
- when Ca2+ binds to troponin, troponin changes conformation which causes the tropomyosin attached to troponin to rotate and expose the binding sites for myosin –>
exposes myosin-binding sites of the actin - Myosin heads can bind to actin
- when myosin head binds the actin, the head changes conformation.
The head bends and and causes a tiny force that causes the actin filament to move 5-10 nm relative to the myosin filament - when a myosin head is bound to actin, it can bind and hydrolyze ATP. The energy released when it binds changes the conformation of the head again and causes it to release the actin and return to its extended position. The head is now ready to a bind with a new actin. ATP helps myosin and actin to dissociate.
- as long as Ca2+ and ATP are available, the cycle of actin and myosin interactions continues and the filaments slide past each other. A Ca2+ active pump (ATP) helps the Ca2+ reuptake in the sarcoplamsic
Contraction steps
- Ca2+ is released from the sarcoplasmic reticulum
- Ca2+ in the sarcoplasm binds troponin and exposes myosin-binding sites on the actin filaments
- myosin heads bind to actin - release of Pi initiates a power stroke
- In the power stroke, the myosin head changes conformation. filaments slide past each other
- ADP is released - ATP binds to myosin, causing it to release actin
- ATP is hydrolyzed. the myosin head returns to its extended conformation
- if Ca2+ is returned to the sarcoplasmic reticulum, the muscle relaxes
- if Ca2+ remains available, the cycle repeats and muscle contraction continues
Ca2+ is released from the
sarcoplasmic reticulum
Ca2+ in the sarcoplasm binds
troponin and exposes myosin-binding sites on the actin filaments
Myosin heads bind to
actin - release of Pi initiates a power stroke
In the power stroke, themyosin head
changes conformation - filaments slide past each other
ADP is release - ATP binds to
myosin, causing it to release actin
If Ca2+ is returned to the
sarcoplasmic reticulum, the muscle relaxes
If Ca2+ remains available
the cycle repeats and muscle contraction continues
