Lidocaine reversibly inhibits fertilization in Chlamydomonas: a possible role for calcium in sexual signalling.

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Abstract
A flagellar adhesion-induced signal sent during the mating reaction of the biflagellate alga, C. reinhardtii, initiates release of cell-wall-degrading enzymes, activation of mating structures and cell fusion. The nature of this signal is unknown, but it may be mediated by an adhesion-induced change (activation) of flagellar tips. Lidocaine, a local anesthetic that is reported to interfere with the movement of divalent cations across cell membranes, reversibly blocks cell wall loss and gametic fusion without blocking adhesion of flagellar tip activation. Lidocaine inhibited the initial rates and the extent of wall loss and zygote formation. Studies with gametes of a paralyzed flagellar mutant, pf 17, revealed that lidocaine also blocked flagellar surface motility (visualized as movement of polystyrene beads) at concentrations of the inhibitor which also prevented gametic fusion. The concentration of lidocaine required to block cell fusion was dependent on the concentration of Ca or Mg in the medium. In the absence of added Ca, 0.5 mM lidocaine inhibited fusion by 70%. In 0.5 mM Ca, 0.5 mM lidocaine had no effect on fusion and 2 mM lidocaine was required for 90% inhibition. Divalent cations may play a critical role in sexual signaling in Chlamydomonas.