Secretory Mechanisms In Paramecium

A Paramecium cell possesses two widely different types of secretory activity. One is the release from dense core secretory organelles, the trichocysts, serving for predator defense by the most rapid known synchronous process: single events lasting <1 ms and <80 ms for the whole population of stimulated cells. The second type is the periodic release of water and excess of ions, notably Ca2+, by the contractile vacuole complex which thus serves for osmoregulation and ionic balance. Trichocyst secretion encompasses organelle docking at regularly placed sites at the cell membrane, with assembly of SNARE proteins and an undefined Ca2+ sensor. Upon stimulation and increase in [Ca2+], membrane fusion and release of contents take place with a speed and synchrony unsurpassed by other dense core vesicle systems. Also exocytosis-endocytosis coupling is relatively fast (<270 ms), so that the entire process takes 350 ms. The apparent time constants are, thus, tau(exo) = 57 ms and tau(endo) = 126 ms; the decay of the cortical Ca2+ signal proceeds with tau = 8 s. Contact with exogenous Ca2+ after exocytotic pore formation triggers automatically explosive decondensation (several-fold elongation of the spindle-shaped trichocyst contents). The two contractile vacuoles are permanently docked at specific sites of the cell membrane. Their membrane fuses with the cell membrane, also at epigenetically predetermined sites, periodically every similar to 10 s, when luminal osmotic pressure has sufficiently increased, probably by mechanosensitive channels enriched by the scaffolding protein, stomatin. Both types of secretory activity depend on local Ca2+ increase. In the case of trichocysts, Ca2+ for membrane fusion is provided by store-operated Ca2+ entry (SOCE) in synchrony with the release of Ca2+ from alveolar sacs, the cortical Ca2+ stores, via ryanodine receptor-like Ca2+-release channels. Remarkably, contractile vacuole complexes also use SNAREs and they are also surrounded by Ca2+ stores, but here the mechanism of [Ca2+](i) increase for membrane fusion remains to be determined.