A colorless euglenoid flagellate Peranema trichophorum shows unique unidirectional gliding cell locomotion on the substratum at velocities up to 30 micro m/s by an as yet unexplained mechanism. In this study, we found that (1) treatment with NiCl(2) inhibited flagellar beating without any effect on gliding movement; (2) water currents applied to a gliding cell from opposite sides caused detachment of the cell body from the substratum. With only the anterior flagellum adhering to the substratum, gliding movement continued along the direction of the anterior flagellum; (3) gentle pipetting induced flagellar severance into various lengths. In these cells, gliding velocity was proportional to the flagellar length; and (4) Polystyrene beads were translocated along the surface of the anterior flagellum. All of these results indicate that a cell surface motility system is present on the anterior flagellum, which is responsible for cell gliding in P. trichophorum.

The first sign of excysting Colpoda cucullus cells is the initiation of the pulsation of a contractile vacuole, which is then replaced by a non-pulsating vacuole (excystment vacuole) that continues to expand and finally ruptures the outermost cyst wall (ectocyst) due to inner pressure. A ciliate surrounded by flexible membranes (endocyst) thus emerges. The osmolarity of the excysting cells is estimated to be 140 mOsm L−1 from the relationship between the frequency of contractile vacuole pulsation and the external sucrose concentration. Both the expansion of the excystment vacuole and the emergence of ciliates occurred even when the cysts were immersed in hypertonic medium. In hypotonic medium containing sodium azide (NaN3, a cytochrome c oxidase inhibitor), the contractile vacuole of vegetative cells stopped pulsating and gradually expanded, causing cells to burst. When C. cucullus was induced to encyst in a hypotonic medium containing NaN3, the expansion of the excystment vacuoles was inhibited. These results suggest that the active uptake of water may be responsible for the expansion of the excystment vacuole required for the ectocyst to rupture.

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The pennate diatom, Bacillaria paxillifer, forms a colony in which adjacent cells glide smoothly and almost continuously, yet no obvious apparatus driving the movement, such as flagella or cilia, is observed. Thus far, neither the mechanism nor physiological significance of this movement has been well understood. Here, we report quantitative analysis of the gliding motion of B. paxillifer and morphological analysis of this diatom with light and electron microscopes. The gliding of pairs of adjacent B. paxillifer cells in a colony was cyclic with rather constant periods while the average gliding period varied from a few seconds to multiples of 10 s among colonies. The gliding was compromised reversibly by inhibitors for actin and myosin, suggesting involvement of the actomyosin system. Indeed, we observed two closely apposed actin bundles near the raphe by fluorescence-labeled phalloidin staining. Using electron microscopy, we observed filamentous structures that resemble the actin bundles seen with fluorescence microscopy, and we also found novel electron-dense structures located between the plasma membrane and these actin-like filaments. From these and other observations, we suggest that B. paxillifer also uses actin bundles and propose a putative myosin as a molecular motor in the gliding of unicellular diatoms.