All or the following are true about excitation contraction coupling except:

Ans. d. Calcium hinds to tropomyosin to initiate muscle contraction (Ref: Guyton 11/e p90)Calcium binds to Troponin C, not to the tropomyosin, to initiate muscle contraction.'The calcium released into the cytosol binds to Troponin C by the actin filaments, to allow cross-bridge cycling, producing force and, in some situations, motion.'Excitation-Contraction CouplingIn skeletal muscle, E-C coupling relies on a direct coupling between key proteins, the sarcoplasmic reticulum (SR) calcium release channel (identified as the ryanodine receptor, RyR) and voltage-gated L-type calcium channels (identified as dihydropyridine receptors, DHPRs).DHPRs are located on the sarcolemma (which includes the surface sarcolemma and the transverse tubules), while the RvRs reside across the SR membrane.The close apposition of a transverse tubule and two SR regions containing RyRs is described as a triad and is predominantly where E-C coupling takes place.E-C coupling proceeds as follows:The membrane potential of a skeletal muscle cell is depolarised by an action potential (e.g. from synaptic activation from an alpha motor neuron)This depolarisation activates voltage-gated DHPRsThis activates RyR type 1 via physical linkage (involving conformational changes that allosterically activates the RyRs)As the RyRs open, calcium is released from the SR into the local junctional space, which then diffuses into the bulk cytoplasm to cause a calcium transient. Note that the SR has a large calcium buffering capacity partially due to a calcium-binding protein called calsequestrin.The calcium released into the cytosol binds to Troponin C by the actin filaments, to allow cross-bridge cycling, producing force and, in some situations, motion.The sarco/endoplasmic reticulum calcium-ATPase (SERCA) actively pumps calcium back into the SR.As calcium declines back to resting levels, the force declines and relaxation occurs.