NON-FILAMENTOUS AQUATIC FUNGI
61
dehydrogenase per cell, relative to isocitric dehydrogenase, are nicely
consistent with the supposed operation of the bicarbonate trigger
mechanism. If it is remembered, further, that isocitritase (needed for
removal of the isocitrate) is synthesized exponentially from the very
start in an RS cell, but that it is not synthesized at all for a good part of
the generation-time of an OC cell (clearly not an example of 'gratuitous'
induction !), the case is greatly strengthened.
The available data can also be examined from a comparative point of
view, taking both OC and RS cells into consideration. When 80% of the
exponential growth phase of an RS cell has been completed, its Q 02 has
been reduced to one-quarter of that of an OC cell at a corresponding
stage in its exponential growth. During these same times, as pointed out
above, the rise in total ketoglutaric dehydrogenase per RS cell does not
keep pace with that of isocitric dehydrogenase. But, this is not so for an
OC cell. The increase in the total activity per cell of both the isocitric
dehydrogenase and the ketoglutaric dehydrogenase is approximately
the same (Lovett and Cantino, 1961). Again, the data are consistent
with the hypothesis regarding the bicarbonate trigger mechanism. We
are dealing, it would seem, not with—or at least not solely with—an
alteration of energy-transforming systems of the cell as an agency for
morphogenesis, but rather an alteration of metabolic pathways as the
focal point for differentiation.
It is important, now, to consider two other crucial questions which
deal with the exponential phase of growth : if the bicarbonate trigger
mechanism operates as proposed, then (a) what is the supply route for
continued generation of ketoglutarate if the latter is continuously,
reductively carboxylated and siphoned off by way of isocitric dehydrogenase, isocitritase, and glycine-alanine transaminase; and (b) how is
the reducing power—specifically, reduced TPN—essential for the process
generated?
With respect to the first of these questions, direct evidence is not
available if we limit ourselves to results derived from synchronized
cultures. However, data are available which suggest that the transformation of glutamate to ketoglutarate represents a one-way system
(Cantino and Horenstein, 1956b), whereon labelled glutamate can lead
to labelled ketoglutarate, but not vice versa. Furthermore, the inference
that the source of supply may stem in part from nitrogenous materials
is consistent with the fact that, during the first 24 hours of exponential
growth, an RS cell does not consume exogenous glucose (Cantino and
Lovett, 1960). With data already available about nitrogen transformations in synchronized cultures of RS cells (Lovett and Cantino, 1960a,
b), it is to be hoped that a solution to this critical question will soon
be forthcoming.
61
dehydrogenase per cell, relative to isocitric dehydrogenase, are nicely
consistent with the supposed operation of the bicarbonate trigger
mechanism. If it is remembered, further, that isocitritase (needed for
removal of the isocitrate) is synthesized exponentially from the very
start in an RS cell, but that it is not synthesized at all for a good part of
the generation-time of an OC cell (clearly not an example of 'gratuitous'
induction !), the case is greatly strengthened.
The available data can also be examined from a comparative point of
view, taking both OC and RS cells into consideration. When 80% of the
exponential growth phase of an RS cell has been completed, its Q 02 has
been reduced to one-quarter of that of an OC cell at a corresponding
stage in its exponential growth. During these same times, as pointed out
above, the rise in total ketoglutaric dehydrogenase per RS cell does not
keep pace with that of isocitric dehydrogenase. But, this is not so for an
OC cell. The increase in the total activity per cell of both the isocitric
dehydrogenase and the ketoglutaric dehydrogenase is approximately
the same (Lovett and Cantino, 1961). Again, the data are consistent
with the hypothesis regarding the bicarbonate trigger mechanism. We
are dealing, it would seem, not with—or at least not solely with—an
alteration of energy-transforming systems of the cell as an agency for
morphogenesis, but rather an alteration of metabolic pathways as the
focal point for differentiation.
It is important, now, to consider two other crucial questions which
deal with the exponential phase of growth : if the bicarbonate trigger
mechanism operates as proposed, then (a) what is the supply route for
continued generation of ketoglutarate if the latter is continuously,
reductively carboxylated and siphoned off by way of isocitric dehydrogenase, isocitritase, and glycine-alanine transaminase; and (b) how is
the reducing power—specifically, reduced TPN—essential for the process
generated?
With respect to the first of these questions, direct evidence is not
available if we limit ourselves to results derived from synchronized
cultures. However, data are available which suggest that the transformation of glutamate to ketoglutarate represents a one-way system
(Cantino and Horenstein, 1956b), whereon labelled glutamate can lead
to labelled ketoglutarate, but not vice versa. Furthermore, the inference
that the source of supply may stem in part from nitrogenous materials
is consistent with the fact that, during the first 24 hours of exponential
growth, an RS cell does not consume exogenous glucose (Cantino and
Lovett, 1960). With data already available about nitrogen transformations in synchronized cultures of RS cells (Lovett and Cantino, 1960a,
b), it is to be hoped that a solution to this critical question will soon
be forthcoming.