76
EDWARD C. CANTINO AND JAMES S. LOVETT
suggestions of higher orders of control. The only obvious alternative is
to explain the regulation of morphogenesis by way of the independent
operation of induction, repression, and feedback on many separate
pathways; this would provide no easy and obvious explanation for the
pleomorphic mutants produced by Blastocladiella.
The mutation of a gene with a capacity for controlling the coordinated morphogenetic response of a cell to an inducer would most
likely lead to pleomorphism. The presence of such a master gene (or
genes) in Blastocladiella
would make the appearance of two, similar,
complex mutants a reasonable expectation. Finally, since any shift in a
delicately balanced and centrally controlled system would most likely
lead to a break-down in co-ordination, the result of a mutation at such
a locus probably would usually be fatal. In fact, one would expect that
very few mutants of this type would ever survive. In B. emersonii, the
rarity of such an event is indicated by (a) the fact that only four
morphological mutants have been detected over a period of 14 years of
intensive day-to-day studies with a single strain; and (b) that in such
mutants, the viability of successive progeny is of the order of magnitude
of only 1% (Cantino and Hyatt, 1953c).
With B. emersonii, direct tests of the above suggestions cannot readily
be made because the fungus does not reproduce sexually—at least not in
a conventional fashion ; thus, ordinary techniques for recombination and
complementation are ruled out. It is possible, however, that advantage
could be taken of (a) the capacity of the spores to form temporary
cytoplasmic bridges with one another, and through which cellular
constituents may be exchanged (Cantino and Horenstein, 1954); or
(b) other 'parasexual' or somatic mechanisms of recombination, if these
can be shown to occur in Blastocladiella
as they do in higher fungi
(Pontecorvo and Kafer, 1958; Raper, 1961). But even in the absence of
recombinational analysis, a great deal could be learned from intentional
production of additional, morphologically incompetent mutants. In this
instance, it would be particularly important to determine whether or
not the altered characters of pleomorphic morphogenetic mutants show
a high incidence of recurrence in identical pathways. Mutants which lack
single specific enzymes directly implicated in the bicarbonate trigger
mechanism would also be very useful. In the long run it may become
difficult to proceed very far beyond the point of demonstrating correlations between biochemical activities and morphogenetic events without
the use of genetically altered strains. In this respect, other sexuallyreproducing, non-filamentous aquatic fungi may begin to play an
important role.
In concluding our discussion of this phase of RS differentiation, it
would be nice, of course, if we could wrap it all up with a tidy explana-
EDWARD C. CANTINO AND JAMES S. LOVETT
suggestions of higher orders of control. The only obvious alternative is
to explain the regulation of morphogenesis by way of the independent
operation of induction, repression, and feedback on many separate
pathways; this would provide no easy and obvious explanation for the
pleomorphic mutants produced by Blastocladiella.
The mutation of a gene with a capacity for controlling the coordinated morphogenetic response of a cell to an inducer would most
likely lead to pleomorphism. The presence of such a master gene (or
genes) in Blastocladiella
would make the appearance of two, similar,
complex mutants a reasonable expectation. Finally, since any shift in a
delicately balanced and centrally controlled system would most likely
lead to a break-down in co-ordination, the result of a mutation at such
a locus probably would usually be fatal. In fact, one would expect that
very few mutants of this type would ever survive. In B. emersonii, the
rarity of such an event is indicated by (a) the fact that only four
morphological mutants have been detected over a period of 14 years of
intensive day-to-day studies with a single strain; and (b) that in such
mutants, the viability of successive progeny is of the order of magnitude
of only 1% (Cantino and Hyatt, 1953c).
With B. emersonii, direct tests of the above suggestions cannot readily
be made because the fungus does not reproduce sexually—at least not in
a conventional fashion ; thus, ordinary techniques for recombination and
complementation are ruled out. It is possible, however, that advantage
could be taken of (a) the capacity of the spores to form temporary
cytoplasmic bridges with one another, and through which cellular
constituents may be exchanged (Cantino and Horenstein, 1954); or
(b) other 'parasexual' or somatic mechanisms of recombination, if these
can be shown to occur in Blastocladiella
as they do in higher fungi
(Pontecorvo and Kafer, 1958; Raper, 1961). But even in the absence of
recombinational analysis, a great deal could be learned from intentional
production of additional, morphologically incompetent mutants. In this
instance, it would be particularly important to determine whether or
not the altered characters of pleomorphic morphogenetic mutants show
a high incidence of recurrence in identical pathways. Mutants which lack
single specific enzymes directly implicated in the bicarbonate trigger
mechanism would also be very useful. In the long run it may become
difficult to proceed very far beyond the point of demonstrating correlations between biochemical activities and morphogenetic events without
the use of genetically altered strains. In this respect, other sexuallyreproducing, non-filamentous aquatic fungi may begin to play an
important role.
In concluding our discussion of this phase of RS differentiation, it
would be nice, of course, if we could wrap it all up with a tidy explana-