ИСТИНА

Mussels are common marine bivalves found in the intertidal and shallow subtidal zones, including the coastal area of White Sea. Their byssal muscles consist solely of smooth muscle fibers. Release of acetylcholine from the excitatory motor neurons causes depolarization of the muscle fibers, an increase in intracellular calcium concentration, and muscle contraction. On the contrary, release of serotonin from the inhibitory neurons causes increase in intracellular cyclic concentration of AMP and muscle relaxation. The anterior byssal retractor muscle (ABRM) is a classic example of a catch smooth muscle, which is able to maintain long tonic contraction with very little energy expenditure. It slowly generates force and remains contracted for long periods after the excitatory input has gone. Some vertebrate smooth muscles are functionally similar to the byssal muscles inasmuch as they contract tonically. Such muscles make up the walls of arterial vessels, bronchi, urethra and some other organs. They also are able to maintain contracted at low energy cost, the phenomenon coined as latch in order to discern it from mussel's catch. Hypertension is the most pivotal case of pathologies that involve and probably arise from disordered latch. To combat these conditions it is essential to learn the molecular basis of latch and how it is regulated. Mussels and ABRM provide useful experimental model, which can be abundantly used for these studies in marine laboratories. The molecular mechanism of catch/latch remains largely unknown. Two current hypotheses will be discussed here. The cross-linking hypothesis is mostly used to explain catch behavior in invertebrates; it implicates a ratchet-like mechanism with molecular pawl such as twitchin. The cross-bridge hypothesis emerges from the latch studies of vertebrate arterial muscles. It proposes that no pawl is needed while actin and myosin form non-cycling cross-bridges that behave as cross-links and have prolonged life-time due to somehow increased affinity. To understand the molecular basis of this phenomena, the structure and composition of molecular motors in mussels and muscles will be discussed, as well as their regulatory mechanisms known to date. A composite model will be discussed that may involve both the latch bridges composed of actin and myosin, and regulatory proteins that associate with actin filaments and act as cross-linkers during tone maintenance.