Ref ID : 579
Andrivon, C.; Membrane control of ciliary movement in ciliates. Biol.Cell 63:133-142, 1988
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Ciliary movement is generated in the axoneme by the unidirectional sliding of the outer doublets of microtubules produced by the adenosine triphosphate (ATP)-energized dynein arms. It is composed of an effective stroke phase and a passive recovery stroke phase. Two parameters are modulated to determine swimming characteristics of the cell (speed and direction): beat frequency; direction of the effective stroke. They are linked to the internal Ca2+ level and to the membrane potential. The membrane governs the internal Ca2+ level by regulating Ca2+ influx and efflux. It contains voltage-sensitive Ca2+ channels through which a passive Ca2+ influx, driven by the electrochemical gradient, occurs during step depolarization. The rise of the Ca2+ level, up to 6.10-7 M triggers ciliary reversal and enhances beat frequency. Ca2+ is extruded from cilia by active transport. Ca2+ also activates a multistep enzymatic process, the first component of which is a membrane calmodulin-dependent guanylate cyclase. cGMP interacts with Ca2+ to modulate the parameters of the ciliary beat. The phosphorylation-dephosphorylation cycle of axoneme and membrane proteins seems to play a major role in controlling ciliary movement. Hyperpolarization of the membrane enhances beat frequency by an unknown mechanism. It could be a modification of the ratio of axonemal bound Ca2+ and Mg2+, or activation by cyclic adenosine monophosphate (cAMP) produced by a membrane adenylate cyclase. The ciliary membrane behaves as a receptor able to detect modifications of external parameters, and as a transductor transmitting the detected signal by a second or third messengers toward the interior of the cilia. These messengers, acting at different levels, modulate the parameters of the mechanism that generates ciliary movement.