Contractile Proteins and Motors Flashcards
What makes muscle cells special
they are cells that have developed the ability to contract which allows for locomotion, body part movement, movement of substances through body
Sacrcolemma
PM of muscle cell
sarcoplasmic reticulum
ER of muscle cell
sarcoplasm
cytoplasm of muscle cell
major proteins involved in muscle contracton
contractile proteins
- myosin
- myofilament (actin)
- tropomyosin
- troponin
myosin family
motor, walks on actin, a lot of types; all but myosin VI walk toward plus end
myosin structure
myosin II (important for our purposes) has 2 heads, neck tail All myosin head domain- ATPase activity, binds actin neck domain- couples with head to move myosin along filament tail domain- confers specific roles for specific myosins
distinguisihing features between different myosins
- divergent c-terminal tail domains
- one and two-headed myosin
- range of activty
Myosin II
- dimeric with two identical heavy chains
- coiled-coil tails pack side by side to form thick filament with heads facing out from the filament
- in skeletal muscle filament is bipolar and referred to as thick filament
microfilaments
actin; two-stranded helical filament; composed of actin subunits; polar; in muscle this is referred to as thin filament because thinner than myosin
ATP bound to actin subunits
important for filament assembly; ATP bound to actin monomers not part of ATP used by myosin during muscle contraction
tropomyosin
rope like actin accessory protein; binds in grooves btwn actin strands
in low Ca2+ binds to actin and blocks myosin binding sites on actin
in high Ca2+ comes off actin and reveals myosin binding sites
Troponin
NOT PRESENT IN SMOOTH MUSCLE
this controls tropomyosin positioning; has three subunits (TN-I, TN-T, TN-C)
TN-C binds Ca2+
Low Ca2+ keeps tropomyosin in position that covers myosin binding site on actin
High Ca2+ binds Ca2+ -> conf change -> movement tropomyosin -> reveals myosin binding site on actin
muscle fiber
muscle cell; long and cylindrical, some of largest cells in body; multinucleate bc formed by fusion of myoblasts; filled w/ multiple mitochondria bc ATP essential for muscle contraction
What makes up muscle cell
Myofibrils= composed of actin and myosin, cytoplasm (sarcoplasm) packed with repeating arrays of filaments (myofibrils); SR wraps around myofibrils; SR is a Ca2+ reservoir
T-tubules
invaginations that transverse inside of cell that are continuous with PM (sarcolemma); function to rapidly transmit action potential from surface membrane to deeply placed myofilaments
terminal cisternae
areas of SR where SR and T-tubules come in close proximity
myofibril structure
composed of actin and myosin filaments in ordered repeating arrangement giving skeletal muscle a striated apperance
sarcomere
repeating contractile units within a myofibril (smallest repeating contractile unit with in myofibril)
Contains two filaments: Thick and thin
Thick filament- myosin filament (contain side by side packing of myosin)
Thin filament- actin filament (contain polymerized/ filamentous actin, tropomyosin, troponin)
Sarcomere microscopically
Dark bands- thick myosin filaments and overlapping thin filaments
Thin bands- thin actin filaments NOT overlapping thick filaments
M line- myosin by itself
Z discs
where plus ends actin filaments attach, define ends of sarcomere, multi protein structure
myofiament arrangment in sarcomere
each thick filament (myosin) is surrounded by 6 thin (actin) filaments
Muscle contraction
- Sarcomere shortens
- Actin and myosin filaments stay same length
- Filaments slide past each other (myosin head links with actin filament which bends the filament and pulls it toward M line) (actin filament slides)
Cross bridge cycle overview
Myosin walks along actin filament (myosin causes actin to slide toward center of sarcomere)
this requires ATP
conformational change in neck (coupled to ATP hydrolysis) which mediates myosin movement
Cross bridge cycle steps
- Released State: myosin binds ATP and comes off actin
- Cocked: myosin hydrolyzes ATP and myosin neck moves, myosin head moves toward actin plus end
- Attached: Myosin tightly binds to actin
- Force generating: free phosphate released (myosin tightly bound to actin), myosin neck moves again pulling head toward actin minus end (power stroke)
- Released State: ADP released, ATP binds head releases from actin, cycle complete
Muscle shortening due to
a lot of actin and myosins simultaneously interactiong not all power strokes at once which is why you have smooth movement not jerky; thousands of sarcomeres shorten in series -> whole muscle shortens; ATP is consumed, force is produced
why does cross bridge cycle slide actin filaments toward center of sarcomere (M-line)
because filaments are tethered to Z discs
Rigor mortis
(Stuck at attached step 4); myosin head lacking bound nucleotide locked tightly onto actin in rigor b/c in death ATP depleted from cells so all myosin heads remain attached to actin, strong physical contact between actin and myosin prevent stretching which makes muscle stiff
What regulates when cross bridge cycling occurs
Ca2+ NOT ATP; can’t use ATP bc no ATP means dead therefore not a good regulator b/c always have to have it
Resting muscle
low cytoplasmic Ca2+; myosin binding site on actin filament blocked by tropomyosin which is held in place by troponin
Activated muscle
High cytoplasmic Ca2+ ->calcium binds to troponin (TN-C) -> myosin binding site exposed on actin filament ->cross bridge cycle occurs
Excitation-contraction (E-C) coupling
link between muscle excitation (depolarization of action potential) to muscle contraction
Ca2+ release skeletal muscle
- Action potential from nerve fiber spreads down T-tubule
- Voltage gated ion channels in sarcolemma activated and change conformation
- Direct physical contact btwn voltage gated channels (in sarcolemma) and Ca2+ release channels in SR -> SR Ca2+ channels opening
- Calcium released from SR into cytoplasm
Skeletal muscle contraction overall
- neuron
- action potential
- voltaged gated ion channel activated
- Ca2+ channel in SR opens
- Ca2+ release from SR into cytoplasm
- calcium binds troponin (TN-C)
- Myosin binding site exposed on actin filament
- Cross bridge cycle
muscle attaches to bone via
tendon
Relaxation of skeletal muscle
- calcium ATPase in SR (SERCA) pumps Ca2+ back into SR lumen
- Ca2+ levels in cytoplasm decrease
- Tropomyosin covers myosin binding site b/c troponin not Ca2+ bound
- Muscle relaxes
Cardiac muscle
striated, has myofilament arrangement; different than skeletal muscle in that Ca2+ channels and voltage gated ion channels not physically linked so activate voltage gated ion channel allowing Ca2+ into sarcoplasm then Ca2+ in sarcoplasm activates Ca2+ receptor on SR and more calcium is released into sarcolemma leading to muscle contraction
(Ca2+ induced Ca2+ release)
Smooth muscle
Not striated because actin and myosin are not organized into distinct bands b/c smooth muscle fx is to maintain tonic contractions and reduce lumen diameter (allows contraction in all directions, has thick and thin filaments just in different direction)
Smooth muscle does NOT contain troponin, calmodulin binds sarcoplasmic calcium in smooth msucle
Calmodulin
binds sarcoplasm calcium in smooth muscle NOT troponin
smooth muscle contactoin
- calmodulin binds calcium in sarcoplasm
- calcium-calmodulin coupled activates myosin light chain kinase (MLCK)
- MCLK phosphorylates myosin
- Phosphorylated myosin binds to actin
- Cross-bridges and filament sliding occurs
- Fiber shortening occurs in all directions
- Dephosphorylation via dephosphorylase of myosin leads to relaxation
muscle cell disruption
can be at contractile protein level, neuronal (electro physical) level, or mitochondrial level
