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assigns the task to the phytoplankton cell itself: that the phytoplankton cell can by itself by
secrete a cell-surface polysaccharide creates and sustains a high ammonium patch in its
microenvironment. The advantage to bacteria would be that they are offered a rich "culture
medium" on the phytoplankton surface.
We should also point out that enriched microenvironments conducive to ammonium release are,
in all probability, not limited to phytoplankton cell surface layers. Particle loci including the
pico- and nano-detritus of appropriate nutritional status may also act as loci for ammonium
release (discussed later).
Implications for phytoplankton aggregation
The phytoplankton-bacteria interactions described above have implications for phytoplankton
aggregation ("marine blizzard" of Smetacek, 1985) as well. Smetacek argues that aggregation
and mass sinking represents a survival strategy: upon sinking, phytoplankton make resting forms
which may be advected back to the surface later and serve as seed populations. We suggest an
alternative hypothesis that, because phytoplankton cells (must) express the surface "mucus"
layer, they have a tendency to aggregate continuously. Bacterial exoenzymes minimize
aggregation by keeping the polymer layer under check. Further, at low cell densities, collision
frequency is low and hence aggregations minimal. Early on in the bloom, aggregation is low
despite high cell density because bacteria keep the phytoplankton surface "enzymatically
pruned". Also during this period, intense N remineralization in the phytoplankter's
microenvironment sustains phytoplankton vitality and growth at the expense of DON. Later, the
utilizable DON runs low due to sinking losses of N, and the bacteria, now in the N-poor but
energy rich polysaccharide layer on the phytoplankton, become competitors and cease to release
ammonium. The N-stressed phytoplankton cells keep secreting polysaccharides, vainly trying to
maintain mutualism (Bratback and Thingstad, 1985), and become sticky, aggregate, and sink.
Bacteria "move in", colonize the mucus, and with their own glues make the aggregates even
more sticky (creating the situation described by Biddanda and Pomeroy, 1988). (Here again one
sees a variable role of bacteria: first they prevent aggregation and later in the bloom they
enhance it).
assigns the task to the phytoplankton cell itself: that the phytoplankton cell can by itself by
secrete a cell-surface polysaccharide creates and sustains a high ammonium patch in its
microenvironment. The advantage to bacteria would be that they are offered a rich "culture
medium" on the phytoplankton surface.
We should also point out that enriched microenvironments conducive to ammonium release are,
in all probability, not limited to phytoplankton cell surface layers. Particle loci including the
pico- and nano-detritus of appropriate nutritional status may also act as loci for ammonium
release (discussed later).
Implications for phytoplankton aggregation
The phytoplankton-bacteria interactions described above have implications for phytoplankton
aggregation ("marine blizzard" of Smetacek, 1985) as well. Smetacek argues that aggregation
and mass sinking represents a survival strategy: upon sinking, phytoplankton make resting forms
which may be advected back to the surface later and serve as seed populations. We suggest an
alternative hypothesis that, because phytoplankton cells (must) express the surface "mucus"
layer, they have a tendency to aggregate continuously. Bacterial exoenzymes minimize
aggregation by keeping the polymer layer under check. Further, at low cell densities, collision
frequency is low and hence aggregations minimal. Early on in the bloom, aggregation is low
despite high cell density because bacteria keep the phytoplankton surface "enzymatically
pruned". Also during this period, intense N remineralization in the phytoplankter's
microenvironment sustains phytoplankton vitality and growth at the expense of DON. Later, the
utilizable DON runs low due to sinking losses of N, and the bacteria, now in the N-poor but
energy rich polysaccharide layer on the phytoplankton, become competitors and cease to release
ammonium. The N-stressed phytoplankton cells keep secreting polysaccharides, vainly trying to
maintain mutualism (Bratback and Thingstad, 1985), and become sticky, aggregate, and sink.
Bacteria "move in", colonize the mucus, and with their own glues make the aggregates even
more sticky (creating the situation described by Biddanda and Pomeroy, 1988). (Here again one
sees a variable role of bacteria: first they prevent aggregation and later in the bloom they
enhance it).