Myosin and Muscle
Muscles are made up of millions of contractile bundles.
chemotactic gradients create zones of Rho activity, Rho is responding to the
Start at Cdc42 (where there's a lot of cyclic-AMP, so there's a lot of Cdc42).
Rho needs to be able to be free to get the job done, so if this wave keeps on going
the back end will start creating lamellipodia
Sarcomeres are the basic unit of the sliding filament theory.
Discovered in 1954
They looked at both EM images of contracting muscles and isolated myofibrils and
watched them contract under microscope. They saw the thickness of the A band or
thick band didn't change.
As the muscle contracted, the length of the I band and sarcomere got shorter.
This implies myosin motors have directionality. And 1960s idea is firmly
Sarcomeres are tightly packed arrays of actin and myosin filaments and undergo rapid
contraction under muscle stimulation.
Contraction is fast!
Only 50ms for a Type-II fibre
5-10ms “latent” period between signal from brain and start of
40-45ms “contraction phase” from fully elongated to fully
contracted. Forming and releasing of these cross-bridges
Not bound to actin filament
Have ATP in myosin head and when myosin binds to ATP, it very rapidly hydrolyzes and the
myosin head goes through conformational change (cocked state)
Cocked state of myosin is a tense state - internal strain
Every non-covalent interaction is strained and it is an uncomfortable state.
Still have ADP and P in the pocket, they are separate entities but stuck in the head
Myosin have high affinity to actin in this state, Myosin head reaches down and binds to the actin filament. After ATP hydrolyzed but before P
Release of P from pocket allows strain to relax and release of that energy that pushes actin
filament out. Produces the power stroke, Myosin has to pop off and a new ATP has to come in.
Release of myosin head from actin come