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PubMed1981

Possible reduction of surface charge by a mutation in Paramecium tetraurelia.

Under voltage clamp, a mutant of Paramecium tetraurelia (teaB) shows a shift in the positive direction of the voltage sensitivity of the Ca conductance and the depolarization inactivation curve by 10 mV with no change in the total conductance. This effect can be mimicked in the wild type by the addition of external CA2+ or Mg2+. The mutation also shifts the resting potential and the voltage sensitivities of the delayed rectification (depolarization-sensitive) K conductance and the anomalous rectification (hyperpolarization-sensitive) K conductance in the positive direction to a similar extent. This systematic shift of channel voltage sensitivities is best explained by the reduction of the surface negative charges of the membrane due to the mutation.

Animals↗
PubMed1986

A mutation that increases a novel calcium-activated potassium conductance of Paramecium tetraurelia.

Under two-electrode voltage clamp, a mutant of P. tetraurelia, restless (rst/rst), showed a large increase in induced current and an outward tail current when compared to the wild-type cell for hyperpolarizing voltage steps. An increase in the induced and tail currents is also observed for depolarizing voltage steps. The larger current during voltage steps and tail in the mutant were eliminated by the use of CsCl-filled electrodes and tetraethylammonium ion (TEA+) in the bath solution, characterizing the lesion as affecting a K+ conductance. Ionophoretic injection of ethylene glycol bis-(beta-aminoethyl ether) n,n,n',n-tetraacetic acid (EGTA) to buffer internal Ca2+ concentration reduced the increased K+ current and tail of the restless cell, indicating Ca2+ activation of the K+ current. Time course and amplitude of remaining currents after blockage of K+ conductances with Cs+ and TEA+ were similar in wild-type and restless cells suggesting no restless defect in entry of calcium. The Ca2+-activated sodium current was similar in the mutant to that in wild type arguing against a defect in calcium regulation activating the K+ channel in the restless cell. We conclude that the restless mutation alters a Ca2+-activated potassium conductance other than the one previously described. The multiplicity of Ca2+-activated potassium conductances in Paramecium is discussed.

Animals↗
PubMed1979

Physiological dissection of various effects of ruthenium red dye on Paramecium cells.

Polycationic dye ruthenium red, but not alcian blue, if externally applied to Paramecium cells quickly inhibits their phagocytosis. Ruthenium red combined with the cell surface diminishes frequency and duration of ciliary reversals and gradually inactivates the Ca++ gating mechanism. This effect persists for 1-3 after ruthenium red removal from the culture medium.

Animals↗
PubMed1986

Primary structure of the Paramecium tetraurelia small-subunit rRNA coding region: phylogenetic relationships within the Ciliophora.

We have sequenced the coding region for the small-subunit rRNA gene from Paramecium tetraurelia. Similarity comparisons between small-subunit rRNAs from representatives of the Metazoa, the Plantae, the Fungi and four other members of the Ciliophora were used to construct phylogenetic trees. In these phylogenies the Ciliophora diverged from the eukaryotic line of descent as a loose phylogenetic grouping during a radiative period that gave rise to the Fungi, the Plantae and the Metazoa.

Animals↗
PubMed1992

Two-state model of Paramecium bursaria thigmotaxis.

A theoretical framework has been developed for analysis of the interaction between Paramecium bursaria and a glass surface. Adhesion to and detachment from a solid substrate were considered in the model as transitions between alternative states in cell behavior: (a) swimming, and (b) motionless (positive thigmotactic) state. According to the model and experimental data, a change in the fraction of swimming cells is described by a negative exponential course. The proposed model allows positive thigmotaxis, generally referred to in the literature simply as thigmotaxis, to be considered as the rate-constant of transition into the motionless state. This approach permits quantitative determination of thigmotaxis, and reveals its dependence on the phase of culture growth and the type of medium surrounding the cells. In the mineral maintenance solution, paramecia from the stationary phase of growth swim more slowly than those in the logarithmic phase of growth, and show enhanced thigmotaxis. However, a general relationship between thigmotaxis and swimming speed was not established.

Animals↗
PubMed1996

Cloning and molecular analysis of the bifunctional dihydrofolate reductase-thymidylate synthase gene in the ciliated protozoan Paramecium tetraurelia.

We have cloned the first bifunctional gene dihydrofolate reductase-thymidylate synthase (DHFR-TS) from a free-living, ciliated protozoan, Paramecium tetraurelia, and determined its macronuclear sequence using a modified ligation-mediated polymerase chain reaction (PCR) that can be of general use in cloning strategies, especially where cDNA libraries are limiting. While bifunctional enzyme sequences are known from parasitic protozoa, none had previously been found in free-living protozoa. The AT-rich (68%) coding region spanning 1386 bp appears to lack introns. DHFR-TS localizes to a approximately 500 kb macronuclear chromosome and is transcribed as an mRNA of approximately 1.66 kb, predicted to encode a 53 kDa protein of 462 residues. The N-terminal one-third of the protein is encoded by DHFR, which is joined by a short junctional peptide of approximately 12 amino acids to the highly conserved C-terminal TS domain. Among known DHFR-TS sequences, the P. tetraurelia gene is most similar to that from Toxoplasma gondii, based on primary sequence and parsimony analyses. The predicted secondary protein structure is similar to those of previously crystallized monofunctional sequences.

Amino Acid Sequence↗
PubMed1999

The gravikinetic response of Paramecium is based on orientation-dependent mechanotransduction.

Paramecium generates persistent shifts of the membrane potential of a few millivolts depending on its orientation with respect to the gravity vector. The resulting potential-induced modulation of the speed of propulsion is called gravikinesis because it acts to neutralize, fully or in part, sedimentation. Gravisensitivity is maximal at neutral orientation, i.e., in horizontally swimming cells, when the gravitational force per unit membrane area is at minimum. Stimulus-response relationships and energetic considerations show that sensing of the gravity vector by a nonspecialized, single-cell organism ranks among the most sensitive mechanoreceptors known in nature.

Animals↗
PubMed2002

Functional and fluorochrome analysis of an exocytotic mutant yields evidence of store-operated Ca2+ influx in Paramecium.

A non-discharge mutant of Paramecium tetraurelia (nd12-35 degrees C, lacking exocytotic response upon stimulation with the nonpermeable polycationic secretagogue aminoethyldextran, AED), in the pawnA genetic context (d4-500r, lacking ciliary voltage-dependent Ca2+ influx), was shown to lack (45)Ca2+ entry from outside upon AED stimulation. In contrast, cells grown at 25 degrees C behave like the wildtype. To check the functional properties in more detail, fluorochrome-loaded 35 degrees C cells were stimulated, not only with AED (EC(100) = 10(-6) M in wildtype cells), but also with 4-chloro-meta-cresol, (4CmC, 0.5 mM), a permeable activator of ryanodine receptor-type Ca2+ release channels, usually at extracellular [Ca2+] of 50 microM, and eventually with a Ca2+ chelator added. We confirm that pwA-nd12(35 degrees C) cells lack any Ca2+ influx and any exocytosis of trichocysts in response to any stimulus. As we determined by x-ray microanalysis, total calcium content in alveolar sacs (subplasmalemmal stores) known to be mobilized upon exocytosis stimulation in wild-type cells, contain about the same total calcium in 35 degrees C as in 25 degrees C cells, and Ca2+ mobilization from alveoli by AED or 4CmC is also nearly the same. Due to the absence of any AED-induced Ca2+ influx in 35 degrees C cells and normal Ca2+ release from stores found by x-ray microanalysis one can exclude a "CICR"-type mechanism (Ca2+-induced Ca2+ release) and imply that normally a store-operated Ca2+ ("SOC") influx would occur (as in 25 degrees C cells). Furthermore, 35 degrees C cells display a significantly lower basal intracellular [Ca2+], so that any increase upon stimulation may be less expressed or even remain undetected. Under these conditions, any mobilization of Ca2+ from stores cannot compensate for the lack of Ca2+ influx, particularly since normally both components have to cooperate to achieve full exocytotic response. Also striking is our finding that 35 degrees C cells are unable to perform membrane fusion, as analyzed with the Ca2+ ionophore, A23187. These findings were corroborated by cryofixation and freeze-fracture analysis of trichocyst docking sites after AED or 4CmC stimulation, which also revealed no membrane fusion. In sum, in nd12 cells increased culture temperature entails multiple defects, notably insensitivity to any Ca2+ signal, which, moreover, cannot develop properly due to a lower basal [Ca2+] level and the lack of Ca2+ influx, despite normal store activation.

Animals↗
PubMed2002

Identification of the Ca2+ conductance responsible for K+-induced backward swimming in Paramecium caudatum.

Membrane potential responses of Paramecium caudatum to an application of K+-rich solution were examined to understand the mechanisms underlying K+-induced backward swimming. A wild-type cell impaled by a microelectrode produced action potentials followed by a sustained depolarization in response to an application of a K+-rich test solution. After termination of the application, a prolongation of the depolarization (depolarizing after-potential) took place. Behavioral mutants incapable of exhibiting K+-induced backward swimming did not show depolarizing afterpotentials. Upon short application of K+-rich solution, the timing and duration of the ciliary reversal of the wild-type cell coincided well with the K+-induced depolarization. The duration of the depolarizing afterpotential decreased as the duration of the application increased. The depolarizing afterpotential recovered slowly after it had been suppressed by a preceding application of the K+-rich solution. By injection of an outward current into the wild-type cell, the action potentials were evoked normally during the period when the K+-induced depolarizing afterpotential was suppressed. We concluded that the prolongation of the depolarizing membrane potential response following the application of the K+-rich solution represents the Ca2+ conductance responsible for the K+-induced backward swimming in P. caudatum and that the characteristics of the K+-induced Ca2+ conductance are distinct from those of the Ca2+ conductance responsible for the action potentials.

Animals↗
PubMed2003

K+-induced Ca2+ conductance responsible for the prolonged backward swimming in K+-agitated mutant of Paramecium caudatum.

The K+-agitated (Kag) mutant of Paramecium caudatum shows prolonged backward swimming in K+-rich solution. To understand the regulation mechanisms of the ciliary motility in P. caudatum, we examined the membrane electrical properties of the Kag mutant. The duration of the backward swimming of the Kag in K+-rich solution was about 10 times longer than that of the wild type. In response to an injection of the outward current, the wild type produced an initial action potential and a subsequent membrane depolarization due to I-R potential drop, while the Kag exhibited repetitive action potentials during the depolarization. Under voltage-clamp conditions, the depolarization-activated transient inward current exhibited by the Kag was slightly smaller than that exhibited by the wild type. In response to an application of K+-rich solution, both the wild type and the Kag exhibited a depolarizing afterpotential representing the activation of the K+-induced Ca2+ conductance. The inactivation time course of the K+-induced Ca2+ conductance of Kag was about 10 times longer than that of the wild type. This difference corresponds well with the difference in behavioral responses between Kag and wild type to K+-rich solution. We conclude that the overreaction of the Kag mutant to the K+-rich solution is caused by slowing down of the inactivation of the K+-induced Ca2+ conductance.

Action Potentials↗
PubMed2004

Temperature-induced change of variant surface antigen expression in Paramecium involves antigen release into the culture medium with considerable delay between transcription and surface expression.

We analyzed temperature-induced changes of variant surface antigen (vsAg) expression in Paramecium primaurelia, using immuno-techniques and mRNA determinations. Upon a 23 degrees C to 33 degrees C shift, the old vsAg, type 156G, remains on the cell surface for a time, when already mRNA for the new form, 156D, is expressed. A considerable amount of 156D-specific mRNA is formed 45-48 h after the temperature shift, while 156D surface expression reaches maximal levels only after >72 h. A new aspect of these experiments is that, during this transition, the old vsAg is steadily released in high-molecular-weight form into the culture medium, as found by dot blot and Western blot analysis of concentrated culture medium. The new vsAg form is first inserted into the somatic cell membrane, before it spreads also into cilia. In the reverse transition, 33 degrees C to 23 degrees C, the adaptation on the level of transcription and surface expression is considerably faster. While we had previously shown, under steady-state conditions (constant temperature), the occurrence of a degradation pathway by endocytotic and phagocytotic ingestion of vsAg this may proceed in parallel to the steady release of old vsAg from the cell surface into the medium. Altogether these combined processes may facilitate the installation of the new vsAg type.

Animals↗
PubMed2000

"Frustrated Exocytosis"--a novel phenomenon: membrane fusion without contents release, followed by detachment and reattachment of dense core vesicles in Paramecium cells.

The lipophilic fluorescent dye, FM1-43, as now frequently used to stain cell membranes and to monitor exo-endocytosis and membrane recycling, induces a cortical [Ca(2+)](i) transient and exocytosis of dense core vesicles ("trichocysts") in Paramecium cells, when applied at usual concentrations (</=10 microm) in presence of extracellular Ca(2+) ([Ca(2+)](o) = 50 microm). When [Ca(2+)](o) is kept at 30 nm (<[Ca(2+)](rest)(i)), in about one third of the population of extrudable trichocysts docked at the cell membrane, FM1-43 induces membrane fusion, visible by FM1-43 fluorescence of the vesicle membrane. However, in this system extrusion of secretory contents cannot occur in absence of any sufficient Ca(2+)(o). Upon readdition of Ca(2+)(o) or some other appropriate Me(2+)(o) at 90 microm, secretory contents can be released (complete exocytosis). Resulting ghosts formed in presence of Ca(2+), Sr(2+) or Mn(2+) are vesicular, but when formed in presence of Mg(2+), for reasons to be elucidated, they are tubular, though both types are endocytosed and lose their FM1-43 stain. In contrast, in presence of [Mg(2+)](o) = 3 mm (which inhibits contents release), the exocytotic openings reseal and intact trichocysts with labeled membranes and with still condensed contents are detached from the cell surface ("frustrated exocytosis") within approximately 15 min. They undergo cytoplasmic streaming and saltatory redocking, with a half-time of approximately 35 min. During this time, the population of redocked trichocysts amenable to exocytosis upon a second stimulus increases with a half-time of approximately 35 min. Therefore, acquirement of competence for exocytotic membrane fusion may occur with only a small delay after docking, and this maturation process may last only a short time. A similar number of trichocysts can be detached by merely increasing [Mg(2+)](o) to 3 mm, or by application of the anti-calmodulin drug, R24517 (calmidazolium). Essentially we show (i) requirement of calmodulin and appropriate [Me(2+)] to maintain docking sites in a functional state, (ii) requirement of Ca(2+)(o) or of some other Me(2+)(o) to drive membrane resealing during exo-endocytosis, (iii) requirement of an "empty" signal to go to the regular endocytotic pathway (with fading fluorescence), and (iv) occurrence of a "filled" signal for trichocysts to undergo detachment and redocking (with fluorescence) after "frustrated exocytosis".

Animals↗
PubMed1997

Facilitation of membrane fusion during exocytosis and exocytosis-coupled endocytosis and acceleration of "ghost" detachment in Paramecium by extracellular calcium. A quenched-flow/freeze-fracture analysis.

We had previously shown that an influx of extracellular Ca2+ (Ca2+e), though it occurs, is not strictly required for aminoethyldextran (AED)-triggered exocytotic membrane fusion in Paramecium. We now analyze, by quenched-flow/freeze-fracture, to what extent Ca2+e contributes to exocytotic and exocytosis-coupled endocytotic membrane fusion, as well as to detachment of "ghosts"-a process difficult to analyze by any other method or in any other system. Maximal exocytotic membrane fusion (analyzed within 80 msec) occurs readily in the presence of [Ca2+]e > or = 5 x 10(-6) M, while normally a [Ca2+]e = 0.5 mM is in the medium. A new finding is that exocytosis and endocytosis is significantly stimulated by increasing [Ca2+]e even beyond levels usually available to cells. Quenching of [Ca2+]e by EGTA application to levels of resting [Ca2+]i or slightly below does reduce (by approximately 50%) but not block AED-triggered exocytosis (again tested with 80 msec AED application). This effect can be overridden either by increasing stimulation time or by readdition of an excess of Ca2+e. Our data are compatible with the assumption that normally exocytotic membrane fusion will include a step of rapid Ca(2+)-mobilization from subplasmalemmal pools ("alveolar sacs") and, as a superimposed step, a Ca(2+)-influx, since exocytotic membrane fusion can occur at [Ca2+]e even slightly below resting [Ca2+]i. The other important conclusion is that increasing [Ca2+]e facilitates exocytotic and endocytotic membrane fusion, i.e., membrane resealing. In addition, we show for the first time that increasing [Ca2+]e also drives detachment of "ghosts"-a novel aspect not analyzed so far in any other system. According to our pilot calculations, a flush of Ca2+, orders of magnitude larger than stationary values assumed to drive membrane dynamics, from internal and external sources, drives the different steps of the exo-endocytosis cycle.

Animals↗
PubMed1998

Caffeine-induced Ca2+ transients and exocytosis in Paramecium cells. A correlated Ca2+ imaging and quenched-flow/freeze-fracture analysis.

Caffeine causes a [Ca2+]i increase in the cortex of Paramecium cells, followed by spillover with considerable attenuation, into central cell regions. From [Ca2+]resti approximately 50 to 80 nm, [Ca2+]acti rises within </=3 sec to 500 (trichocyst-free strain tl) or 220 nm (nondischarge strain nd9-28 degrees C) in the cortex. Rapid confocal analysis of wildtype cells (7S) showed only a 2-fold cortical increase within 2 sec, accompanied by trichocyst exocytosis and a central Ca2+ spread during the subsequent >/=2 sec. Chelation of Ca2+o considerably attenuated [Ca2+]i increase. Therefore, caffeine may primarily mobilize cortical Ca2+ pools, superimposed by Ca2+ influx and spillover (particularly in tl cells with empty trichocyst docking sites). In nd cells, caffeine caused trichocyst contents to decondense internally (Ca2+-dependent stretching, normally occurring only after membrane fusion). With 7S cells this usually occurred only to a small extent, but with increasing frequency as [Ca2+]i signals were reduced by [Ca2+]o chelation. In this case, quenched-flow and ultrathin section or freeze-fracture analysis revealed dispersal of membrane components (without fusion) subsequent to internal contents decondensation, opposite to normal membrane fusion when a full [Ca2+]i signal was generated by caffeine stimulation (with Ca2+i and Ca2+o available). We conclude the following. (i) Caffeine can mobilize Ca2+ from cortical stores independent of the presence of Ca2+o. (ii) To yield adequate signals for normal exocytosis, Ca2+ release and Ca2+ influx both have to occur during caffeine stimulation. (iii) Insufficient [Ca2+]i increase entails caffeine-mediated access of Ca2+ to the secretory contents, thus causing their decondensation before membrane fusion can occur. (iv) Trichocyst decondensation in turn gives a signal for an unusual dissociation of docking/fusion components at the cell membrane. These observations imply different threshold [Ca2+]i-values for membrane fusion and contents discharge.

Animals↗
PubMed1998

Evidence for two separate purinergic responses in Paramecium tetraurelia: XTP inhibits only the oscillatory responses to GTP.

The purine nucleotide GTP causes a complex behavioral response and two distinct electrophysiological responses in the ciliated protozoan Paramecium tetraurelia. One of the two electrophysiological responses is an oscillating current that is responsible for the repeated backward swimming episodes that constitute the behavioral response to GTP. The second electrophysiological response is a sustained current whose relationship to the first is unknown. Here we show that the purine nucleotides XTP can completely block both the behavioral response to GTP and its associated oscillating current, but not the sustained current induced by GTP. Notably, XTP alone causes a sustained current similar to that induced by GTP. We believe the data support the notion that P. tetraurelia possesses two distinct signal transduction pathways sensitive to purine nucleotides: one specific for GTP that leads to oscillating currents and behavior, and a second pathway activated by GTP and other purine nucleotides that leads to a sustained current.

Animals↗
PubMed1999

Veratridine-mediated Ca2+ dynamics and exocytosis in paramecium cells.

We analyzed [Ca2+]i transients in Paramecium cells in response to veratridine for which we had previously established an agonist effect for trichocyst exocytosis (Erxleben & Plattner, 1994. J. Cell Biol. 127:935-945; Plattner et al., 1994. J. Membrane Biol. 158:197-208). Wild-type cells (7S), nondischarge strain nd9-28 degrees C and trichocyst-free strain "trichless" (tl), respectively, displayed similar, though somewhat diverging time course and plateau values of [Ca2+]i transients with moderate [Ca2+]o in the culture/assay fluid (50 microM or 1 mm). In 7S cells which are representative for a normal reaction, at [Ca2+]o = 30 nm (c.f. [Ca2+]resti = approximately 50 to 100 nm), veratridine produced only a small cortical [Ca2+]i transient. This increased in size and spatial distribution at [Ca2+]o = 50 microM of 1 mm. Interestingly with unusually high yet nontoxic [Ca2+]o = 10 mm, [Ca2+]i transients were much delayed and also reduced, as is trichocyst exocytosis. We interpret our results as follows. (i) With [Ca2+]o = 30 nm, the restricted residual response observed is due to Ca2+ mobilization from subplasmalemmal stores. (ii) With moderate [Ca2+]o = 50 microM to 1 mm, the established membrane labilizing effect of veratridine may activate not only subplasmalemmal stores but also Ca2+o influx from the medium via so far unidentified (anteriorly enriched) channels. Visibility of these phenomena is best in tl cells, where free docking sites allow for rapid Ca2+ spread, and least in 7S cells, whose perfectly assembled docking sites may "consume" a large part of the [Ca2+]i increase. (iii) With unusually high [Ca2+]o, mobilization of cortical stores and/or Ca2+o influx may be impeded by the known membrane stabilizing effect of Ca2+o counteracting the labilizing/channel activating effect of veratridine. (iv) We show these effects to be reversible, and, hence, not to be toxic side-effects, as confirmed by retention of injected calcein. (v) Finally, Mn2+ entry during veratridine stimulation, documented by Fura-2 fluorescence quenching, may indicate activation of unspecific Me2+ channels by veratridine. Our data have some bearing on analysis of other cells, notably neurons, whose response to veratridine is of particular and continuous interest.

Animals↗
PubMed2001

Fluid phase and receptor-mediated endocytosis in Paramecium primaurelia by fluorescence confocal laser scanning microscopy.

In ciliated protozoa, most nutrients are internalized via phagocytosis by food vacuole formation at the posterior end of the buccal cavity. The uptake of small-sized molecules and external fluid through the plasma membrane is a localized process. That is because most of the cell surface is internally covered by an alveolar system and a fibrous epiplasm, so that only defined areas of the cell surface are potential substance uptake sites. The purpose of this study is to analyze, by fluorescence confocal laser scanning microscopy, the relationship between WGA (Triticum vulgaris agglutinin) and dextran internalization in Paramecium primaurelia cells blocked in the phagocytic process, so that markers could not be internalized via food vacuole formation. WGA, which binds to surface constituents of fixed and living cells, was used as a marker for membrane transport and dextran as a marker for fluid phase endocytosis. After 3 min incubation, WGA-FITC is found on plasma membrane and cilia, and successively within small cytoplasmic vesicles. After a 10-15 min chase in unlabeled medium, the marked vesicles decrease in number, increase in size and fuse with food vacuoles. This fusion was evidenced by labeling food vacuoles with BSA-Texas red. Dextran enters the cell via endocytic vesicles which first localize in the cortical region, under the plasma membrane, and then migrate in the cytoplasm and fuse with other endocytic vesicles and food vacuoles. When cells are fed with WGA-FITC and dextran-Texas red at the same time, two differently labeled vesicle populations are found. Cytosol acidification and incubation in sucrose medium or in chlorpromazine showed that WGA is internalized via clathrin vesicles, whereas fluid phase endocytosis is a clathrin-independent process.

Animals↗
PubMed1997

Toxic effects of antimalarial drugs in Paramecium: role of calcium channels.

The antimalarial drugs, quinacrine, quinine and mefloquine, as well as the structurally-similar compound, W-7, inhibit calcium-dependent backward swimming and calcium currents in Paramecium calkinsi. These drugs are also toxic to paramecia at high concentrations. Therefore, one site of toxic action of the drugs may be the calcium channel. To test this hypothesis, the toxicity of the antimalarials and W-7 was compared in paramecia with and without calcium channels. Since calcium channels are located on the cilia, calcium channels were removed from the paramecia by deciliating the cells. Deciliated cells were found to be less susceptible to the lethal effects of the antimalarials and W-7 than their ciliated counterparts. Moreover, Pawns, mutants of P. tetraurelia that possess cilia but lack functional calcium channels, were also less susceptible to the antimalarials than wild-type cells. Thus, calcium channels may be one site of toxic action of the antimalarial drugs in paramecia and perhaps in other protists.

Animals↗