NON-FI LAMENTO US AQUATIC FUNGI
65
when such cells are induced to consume additional bicarbonate14
C at
twice their normal rate (Cantino and Horenstein, 1956a), the total
soluble pool of labelled succinate within the cells also doubles. Let us
assume, then, that a transient rise in the pool of ketoglutarate and/or
succinate also occurs when synchronized OC cells begin to develop
exponentially in bicarbonate media. Do succinate and/or ketoglutarate,
then, function as inducers for the established rise and fall of enzyme
systems such as isocitritase, isocitric dehydrogenase and ketoglutarate
dehydrogenase during exponential growth?
Many of the discriminative experiments which have been devised to
test this sort of thing in other organisms have not been tried yet on
Blastocladiella]
but, with the equally elegant test system that a
synchronized, single-generation culture provides, no doubt they will be
tried. In the meantime, since it seems likely to us that accumulation of
succinate and ketoglutarate govern the formation and/or the activity of
isocitritase and ketoglutaric dehydrogenase, let us consider their
possible mode of action.
In Rhodopsevdomonas,
for example, synthesis of isocitritase is
suppressed by succinate (Kornberg and Lascelles, 1960; see also
Kornberg et ah, 1960), a direct product of the enzymatic reaction which
it mediates. This is not inconsistent with the notion that feedback
inhibition often involves (Pardee, 1961) the action of a repressor which
is generally at the end of an unbranched path in which the enzyme
actually repressed is near the beginning. Relative to such systems, the
question has also been raised (Lester and Yanofsky, 1961): do some
inducers of enzyme formation also inhibit synthesis of repressors
themselves (or antagonize them; Pardee et al., 1958; Kunkee, 1960a, b)
rather than affect directly the formation of the enzyme? Indeed, to
return to our starting point, it has been suggested (Kornberg et al., 1960)
that succinate levels may govern both activity and formation of
isocitritase.
In the system with which we are presently concerned in Blastocladiella,
succinate is the end-product of both of the enzymes so markedly affected
by bicarbonate—namely, isocitritase and ketoglutaric dehydrogenase.
If succinate can control synthesis and activity of isocitritase, perhaps it
can also govern the activity and/or formation of some part of the
ketoglutaric dehydrogenase complex. But, how should one resolve the
dilemma which results : the apparent synthesis—at least the accumulation of total activity—of isocitritase per cell is increased, while simultaneously, that of ketoglutaric dehydrogenase is rapidly curtailed.
Perhaps a partial answer lies in the architecture of the cell.
The 'feeder' reaction of glycolysis may be tightly bound to mitochondria and microsomes (Crane and Sols, 1953), with other glycolytic
65
when such cells are induced to consume additional bicarbonate14
C at
twice their normal rate (Cantino and Horenstein, 1956a), the total
soluble pool of labelled succinate within the cells also doubles. Let us
assume, then, that a transient rise in the pool of ketoglutarate and/or
succinate also occurs when synchronized OC cells begin to develop
exponentially in bicarbonate media. Do succinate and/or ketoglutarate,
then, function as inducers for the established rise and fall of enzyme
systems such as isocitritase, isocitric dehydrogenase and ketoglutarate
dehydrogenase during exponential growth?
Many of the discriminative experiments which have been devised to
test this sort of thing in other organisms have not been tried yet on
Blastocladiella]
but, with the equally elegant test system that a
synchronized, single-generation culture provides, no doubt they will be
tried. In the meantime, since it seems likely to us that accumulation of
succinate and ketoglutarate govern the formation and/or the activity of
isocitritase and ketoglutaric dehydrogenase, let us consider their
possible mode of action.
In Rhodopsevdomonas,
for example, synthesis of isocitritase is
suppressed by succinate (Kornberg and Lascelles, 1960; see also
Kornberg et ah, 1960), a direct product of the enzymatic reaction which
it mediates. This is not inconsistent with the notion that feedback
inhibition often involves (Pardee, 1961) the action of a repressor which
is generally at the end of an unbranched path in which the enzyme
actually repressed is near the beginning. Relative to such systems, the
question has also been raised (Lester and Yanofsky, 1961): do some
inducers of enzyme formation also inhibit synthesis of repressors
themselves (or antagonize them; Pardee et al., 1958; Kunkee, 1960a, b)
rather than affect directly the formation of the enzyme? Indeed, to
return to our starting point, it has been suggested (Kornberg et al., 1960)
that succinate levels may govern both activity and formation of
isocitritase.
In the system with which we are presently concerned in Blastocladiella,
succinate is the end-product of both of the enzymes so markedly affected
by bicarbonate—namely, isocitritase and ketoglutaric dehydrogenase.
If succinate can control synthesis and activity of isocitritase, perhaps it
can also govern the activity and/or formation of some part of the
ketoglutaric dehydrogenase complex. But, how should one resolve the
dilemma which results : the apparent synthesis—at least the accumulation of total activity—of isocitritase per cell is increased, while simultaneously, that of ketoglutaric dehydrogenase is rapidly curtailed.
Perhaps a partial answer lies in the architecture of the cell.
The 'feeder' reaction of glycolysis may be tightly bound to mitochondria and microsomes (Crane and Sols, 1953), with other glycolytic