NON-FILAMENTOUS AQUATIC FUNGI
75
the hypothesis, however, required demonstration that a change in
morphology depends upon the activity of these enzymes in a manner
consistent with prediction. One unequivocal manner of displaying such
dependence in any organism makes use of mutant strains. The discriminating power of this approach in the analysis of cellular control
mechanisms has been amply demonstrated, for example, in bacteria
(Jacob and Monod, 1961a, b ; Neidhardt, 1960 ; Yarmolinsky et ah, 1961).
In this direction, a start has also been made by the analysis of two,
morphologically incompetent mutants of Blastocladiella, each of which
appeared spontaneously in separate, wild-type strains of the fungus
(Cantino, 1953; Cantino and Hyatt, 1953b, c). Both mutants lack a
key enzyme, a-ketoglutaric dehydrogenase (as well as aconitase),
essential to the proposed mechanism (Fig. 6) ; both contain carotene, like
RS cells but unlike typical OC cells; both produce thin-walled cells
automatically, while neither of them can be induced to form thick-walled
RS cells with bicarbonate, nor do they do so spontaneously. The loss in
capacity of these mutants to respond to the bicarbonate inducer—so
effective with the wild-type—provides additional evidence for the
morphogenetic importance of ketoglutaric dehydrogenase. However, the
fact that deletion of this enzyme is accompanied by other changes (loss
in aconitase, appearance of carotene) precludes any simple, cause-andeffect interpretation concerning its role in differentiation.
From an altogether different point of view, the near identity of all
characteristics associated with these two mutants, which appeared
independently at different times, is very striking. The origin of two such
similar, complex phenotypes could have resulted either from a simultaneous and identical mutation of two or more genes in each strain, or
by one mutation in a single pleotropic gene. The first of these, though
possible, is nonetheless most improbable on statistical grounds. In
contrast, particularly in the light of recent work on microbial genetics,
the second alternative seems to us to be the most provocative. If the
mechanisms proposed by Jacob and Monod (1961a, b) for genetic control
of enzyme induction and repression are correct, and if we take the liberty
to apply them to our supposedly more advanced (but still quite lowly)
aquatic fungi, then it seems reasonable to postulate that some kind of
regulator gene must account for the origin of these mutants. This
hypothetical gene might be responsible for the orderly integration of the
cell's response to the bicarbonate inducer (and/or some product resulting
from its action). The steadily-accumulating evidence in the literature
for single genes which can control the co-ordinate induction or repression
of sequential enzymes in biosynthetic or degradative pathways (Buttin,
1961; Hartman et al, 1960; Jacob and Monod, 1961a, b; Vogel, 1961;
Yarmolinsky et al., 1961; Monod and Jacob, 1961) lends support to
75
the hypothesis, however, required demonstration that a change in
morphology depends upon the activity of these enzymes in a manner
consistent with prediction. One unequivocal manner of displaying such
dependence in any organism makes use of mutant strains. The discriminating power of this approach in the analysis of cellular control
mechanisms has been amply demonstrated, for example, in bacteria
(Jacob and Monod, 1961a, b ; Neidhardt, 1960 ; Yarmolinsky et ah, 1961).
In this direction, a start has also been made by the analysis of two,
morphologically incompetent mutants of Blastocladiella, each of which
appeared spontaneously in separate, wild-type strains of the fungus
(Cantino, 1953; Cantino and Hyatt, 1953b, c). Both mutants lack a
key enzyme, a-ketoglutaric dehydrogenase (as well as aconitase),
essential to the proposed mechanism (Fig. 6) ; both contain carotene, like
RS cells but unlike typical OC cells; both produce thin-walled cells
automatically, while neither of them can be induced to form thick-walled
RS cells with bicarbonate, nor do they do so spontaneously. The loss in
capacity of these mutants to respond to the bicarbonate inducer—so
effective with the wild-type—provides additional evidence for the
morphogenetic importance of ketoglutaric dehydrogenase. However, the
fact that deletion of this enzyme is accompanied by other changes (loss
in aconitase, appearance of carotene) precludes any simple, cause-andeffect interpretation concerning its role in differentiation.
From an altogether different point of view, the near identity of all
characteristics associated with these two mutants, which appeared
independently at different times, is very striking. The origin of two such
similar, complex phenotypes could have resulted either from a simultaneous and identical mutation of two or more genes in each strain, or
by one mutation in a single pleotropic gene. The first of these, though
possible, is nonetheless most improbable on statistical grounds. In
contrast, particularly in the light of recent work on microbial genetics,
the second alternative seems to us to be the most provocative. If the
mechanisms proposed by Jacob and Monod (1961a, b) for genetic control
of enzyme induction and repression are correct, and if we take the liberty
to apply them to our supposedly more advanced (but still quite lowly)
aquatic fungi, then it seems reasonable to postulate that some kind of
regulator gene must account for the origin of these mutants. This
hypothetical gene might be responsible for the orderly integration of the
cell's response to the bicarbonate inducer (and/or some product resulting
from its action). The steadily-accumulating evidence in the literature
for single genes which can control the co-ordinate induction or repression
of sequential enzymes in biosynthetic or degradative pathways (Buttin,
1961; Hartman et al, 1960; Jacob and Monod, 1961a, b; Vogel, 1961;
Yarmolinsky et al., 1961; Monod and Jacob, 1961) lends support to