We may return, briefly, to the ability of live phytoplankton, especially diatoms, to exercise this further control on their own sinking rates below that expected from a modified Stokes equation, with all components properly evaluated. It has to be confirmed first that we use a correct interpretation of facts. Smayda (1970) referred to the acceleration of sinking rates in moribund diatoms, and the several mechanisms by which this might come about. These include the aggregation of dying cells and, through their involvement with other planktic detritus (zooplankton exuviae and faecal fragments, colloidal organ-ics, fragments of plant remains), their formation in to larger floccular particles, collectively known as 'marine snow' (Alldredge and Silver, 1988). In these aggregates, particles may sink faster than might be predicted if they were separated. However, the consistency and reproducibil-ity of behaviour of killed cells having similar form resistance should prompt us to regard this as the 'normal' sinking performance and to ask how it might be that live, healthy cells reduce their sinking rates below those that Stokes' law would predict.
The scale of these reductions is impressive, the 'live' rate being up to one order of magnitude, and frequently two- to four-fold less than the 'killed' rate. As well as the case of Stephano-discus rotula illustrated in Fig. 2.8, there is an abundance of data to show the sinking rates of healthy, eight-celled Asterionella formosa colonies to be typically 2-3 ¡m s-1 (about 0.2-0.3 m d-1) rather than the 7-8 ¡m s-1 explained by the modified Stokes' equation (Smayda, 1974; Tilman and Kilham, 1976; Jaworski et al., 1981; Wiseman and Reynolds, 1981). Similarly, variations in the sinking rate of Fragilaria crotonensis may be <0.4 m d-1 for long periods but quite quickly increase to up to 1.1m d-1 (<13 ¡m s-1) when cells are nutrient limited or have been exposed to excessive sunlight (Reynolds, 1973a, 1983a). Indeed, these studies have suggested that it is a useful biological adaptation for an otherwise non-motile organism to be able to increase sinking rate spontaneously and to 'accelerate out of danger' from excessive irradiance, especially in stabilising water columns (Reynolds et al., 1986).
It might appear that regulation of sinking rate is under the control of the diatom. Certainly, variability in the number of cells per colony may be, to an extent, self-regulated as the intercellular links vary in structure, some being much more amenable to separation than others. The frequency of 'linking valves' and 'separation valves'
varies interspecifically. It is not known whether the form of the valves responds to environmental control, so making it possible to build longer chains and filaments or shorter ones, according to circumstances. Many papers refer to varying numbers of cells per coenobium during growth and senescence, perhaps speculating on the role of nutrient limitation. Observations on many natural populations and of isolates treated in the laboratory leads me to the view that coenobia are larger (i.e. comprise more cells) if grown rapidly in unshaken cultures but are more fragmented in old cultures, with many moribund cells. These clearly make some impact on sinking rate but, as we have shown already, these are relatively small compared to the sinking-rate variations attributable to changes in the physiological vitality of the cells.
The physiological mechanisms regulating sinking rate remain stubbornly resistant to explanation. Over a number of years, colleagues at the Ferry House supported my efforts to develop a plausible hypothesis for this behaviour. It is not an entirely negative outcome to say that these succeeded only in excluding several possibilities. We never found a sufficient or sufficiently responsive variation in density that would explain a two- or three-fold change in sinking rate. While we were able to bring pressure to bear on planktic Cyanobacteria to collapse gas vesicles, to subject diatoms to similar treatment - up to about 12 bars, anyway - produced no response at all. Yet if sufficient of the specific photosyn-thetic inhibitor DCMU [3-(3,4-dichlorophenyl)-1,1-dimethyl urea] is added to a healthy, slow-sinking suspension of Asterionella cells to block their photosynthesis, sinking rate rose quickly to the rates of killed or moribund examples. In time, both effects are reversible (photosynthetic capacity, sinking-rate control are recovered). Contemporaneous work in our laboratory on the susceptibility of Asterionella formosa to attack by parasitic fungi (see especially Canter and Jaworski, 1981) had just revealed that, under conditions of low light or darkness, infective chytrid zoospores are not attracted to Asterionella cells as they are in the light. We deduced that actively photosynthesising cells either broadcast a signal to the adjacent medium advertising their presence or that they create a local change in the medium that is exploited or avoided by the infective spores. The lateral thinking that arose from our discussions led to the hypothesis that photosynthesising cells were immobilising water around their periphery. Thus, the particle acquires a new identity and the new dimensions of alga + water, in much the similar way that an investment of mucilage provides (see Section 2.5.2).
Considering that a sufficient swathe of mucilage has not been observed in these algae, the candidate mechanism that we proposed was that the surface charge on the cells was variable and that this might affect the amount of water thus immobilised. This was not an original inspiration but an echo of an earlier hypothesis, put forward by Margalef (1957). Based on his own observations of differing polarity and electro-kinetic ('zeta') potential of Scenedesmus cells, he developed a theory of 'structural viscosity', where algae regulated the viscosity of their immediate surroundings through the electrical charge on the outer cell wall. It must be emphasised that, like any other small particles dispersed in an electrolyte (albeit, a very weak one), algae carry a surface charge in any case. This is, in part, determined by the ionic strength of the medium. Moreover, several publications detailing direct measurements of surface charge using electrophoretic procedures were available (Ives, 1956; Griinberg, 1968; Hegewald, 1972; Zhurav-leva and Matsekevich, 1974). It became our objective to demonstrate that variable sinking rates are related to physiologically mediated changes in surface charge. We used an electrophore-sis microscope to determine simultaneously the sinking rates and electrophoretic mobility of Asterionella colonies, incubated under varying laboratory conditions (Wiseman and Reynolds, 1981). The outcome was quite clear, insofar as large changes in sinking rate could not be correlated with relatively small variations in surface charge. The experiments succeeded only in rejecting another hypothesis about sinking-rate regulation and in establishing a nice method for the direct measurement of sinking rates.
The (as yet) unexplored alternative hypothesis we put forward (Wiseman and Reynolds, 1981) referred to a quite different role for mucilage, that it might be trailed in threads from cells, like a parachute or in the manner of the chitin hairs of Thalassiosira. Unlike chitin, threads of mucilage require active maintenance by healthy cells but would be sufficiently frail to be shed quickly, when they become a liability or too costly to maintain. Traditional algal anatomists would concur in conversation that such mucilaginous threads and trails exist but there seems very little published to uphold a compelling case. Even the use of Indian-ink irrigation, a popular technique for revealing mucilaginous structures, has proved unhelpful to the argument. However, a recent description of mucilaginous protuberances radiating from the marginal cells of Pediastrum duplex colonies (Krienitz, 1990) has been confirmed in the photomicrographs of Padisak et al. (2003a).
Back in the 1980s, we had proposed a number of approaches to investigate the hypothesis, including the possibility of using WETSTEM electron microscopy, for the observation of living materials at high magnification, which was then just becoming available. However, this was also the time when the sponsorship of science was moving rapidly from academic, curiosity-led problems such as this. Purchase or lease of suitable apparatus was less the problem than was the continued support to sustain an active group of personnel. Resolution of the mechanism of vital regulation of sinking rate by diatoms remains open to future research.
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