Mechanical stimulation activates beating in calcium-arrested lateral cilia ofMytilus edulis gill

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Abstract
Lateral cilia ofMytilus edulis gill arrest upon mechanical stimulation, the result of calcium influx. A mechanical stimulus that deflects these cilia toward the effective stroke, and is normally sufficient to cause transient arrest in beating lateral cilia or transient movement into the recovery stroke in quiescent cilia, initiates beating in Ca2+ ionophore-arrested cilia at 9–15 Hz, for periods as long as 30 S. This movement is restricted to the stimulated cilia and the beat pattern appears constrained in the first half of the beat cycle. Application of dopamine causes ciliary arrest in the presence (but not absence) of Ca2+ and mechanical stimulation will also activate such cilia to beat. In the presence of ATP, mechanical stimulation of detergent-permeabilized lateral cell models arrested in the presence of 50 μm Ca2+ will also cause activation comparable in frequency, duration, and beat pattern to that seen in Ca2+-arrested cells, but the initiation is more difficult. Upon application of ionophore in Ca2+-free (EGTA) seawater, the cilia become quiescent, stopped at the end of the recovery stroke. Mechanical stimulation will cause activation of beat, with a similar range of frequencies and duration as in Ca2+-arrested lateral cilia, but the beat pattern is normal and cilia of adjacent cells may also beat, presumably initiated by mechanical coupling. Gently lifting cilia at their basal ends, using small, slow movements of a mechanical probe, will initiate several beat cycles in quiescent lateral cilia but will cause Ca2+-arrested cilia to‘snap’ into the effective stroke and back. These data indicate that Ca2+-arrest does not involve permanent, rigor-like dynein crossbridges since such cilia are quite capable of beating, if given sufficient momentum. This would also suggest that ionic control must act at the level of crossbridge initiation, timing or coordination.