THE ACRASINA
159
static a picture; but it should be borne in mind that antigen-antibody
bonds, in theory at least, can be made and broken repeatedly. Curtis
(1960), however, has raised objections to the existence of any form of
specific bonding, but though his rheological alternative may explain
many phenomena, it is doubtful whether it shows sufficient specificity.
Gregg (1956) found that antisera against two Dictyostelium species
agglutinated heterologous amoebae only from older cultures. He concluded that new surface antigens common to all species tested appeared
during development and were probably but not necessarily concerned
with adhesion; and he believed his data supported the Tyler-Weiss
hypothesis, though of course it would have been much more difficult to
demonstrate complementary substances, even if they existed. However,
it is surprising that these antigens appeared during the logarithmic
growth phase, if they really were responsible for adhesion during aggregation. The significance of these results is further obscured by the fact
that though the cells used in producing antisera had been aggregating
or were about to do so, just before injection they were centrifuged in
distilled water; they would consequently have lost some material, and
been rendered nonadhesive and unable to reaggregate without considerable delay (Section III, B). Moreover, the test cells, which had been
similarly treated, no longer showed the spontaneous agglutination
which Gerisch (1960) found to be as intense, at all ages, as that induced
by antisera.
Nevertheless, serology provides a most delicate tool for studying
rapid and radical surface changes, and it would be interesting to expose
cells left in situ, and therefore of determinate state, to labelled antiserum from which antibodies reacting with antigens present at earlier
stages had been removed by absorbing them on 'younger' cells. However,
I have experienced considerable difficulty in producing antisera to aggregating cells, because of the lability of this condition. Even if the cells
are allowed time to aggregate in water after being centrifuged free from
bacteria, at 37° C they immediately round up and detach themselves
from one another before dying; and since this change may be prevented
by 2-4-dinitrophenol poisoning, it may well involve altering adhesive
material. It is interesting that Moscona (1961) has reported that some
vertebrate cells adhere when cultured at 37° but not at 15°.
Gregg and Trygstad (1958) found that the surface antigens of two of
Sussman's aggregateless mutants differed from those of the wild strain
and other such mutants. One may wonder whether the acrasin receptor
was affected, as these two were the ones that were not attracted by
aggregations (Ennis and Sussman, 1958a). But if adhesion in aggregation does depend on an antigenic change, the wild strain should differ
from all aggregateless ones, and it would thus be profitable to try to
159
static a picture; but it should be borne in mind that antigen-antibody
bonds, in theory at least, can be made and broken repeatedly. Curtis
(1960), however, has raised objections to the existence of any form of
specific bonding, but though his rheological alternative may explain
many phenomena, it is doubtful whether it shows sufficient specificity.
Gregg (1956) found that antisera against two Dictyostelium species
agglutinated heterologous amoebae only from older cultures. He concluded that new surface antigens common to all species tested appeared
during development and were probably but not necessarily concerned
with adhesion; and he believed his data supported the Tyler-Weiss
hypothesis, though of course it would have been much more difficult to
demonstrate complementary substances, even if they existed. However,
it is surprising that these antigens appeared during the logarithmic
growth phase, if they really were responsible for adhesion during aggregation. The significance of these results is further obscured by the fact
that though the cells used in producing antisera had been aggregating
or were about to do so, just before injection they were centrifuged in
distilled water; they would consequently have lost some material, and
been rendered nonadhesive and unable to reaggregate without considerable delay (Section III, B). Moreover, the test cells, which had been
similarly treated, no longer showed the spontaneous agglutination
which Gerisch (1960) found to be as intense, at all ages, as that induced
by antisera.
Nevertheless, serology provides a most delicate tool for studying
rapid and radical surface changes, and it would be interesting to expose
cells left in situ, and therefore of determinate state, to labelled antiserum from which antibodies reacting with antigens present at earlier
stages had been removed by absorbing them on 'younger' cells. However,
I have experienced considerable difficulty in producing antisera to aggregating cells, because of the lability of this condition. Even if the cells
are allowed time to aggregate in water after being centrifuged free from
bacteria, at 37° C they immediately round up and detach themselves
from one another before dying; and since this change may be prevented
by 2-4-dinitrophenol poisoning, it may well involve altering adhesive
material. It is interesting that Moscona (1961) has reported that some
vertebrate cells adhere when cultured at 37° but not at 15°.
Gregg and Trygstad (1958) found that the surface antigens of two of
Sussman's aggregateless mutants differed from those of the wild strain
and other such mutants. One may wonder whether the acrasin receptor
was affected, as these two were the ones that were not attracted by
aggregations (Ennis and Sussman, 1958a). But if adhesion in aggregation does depend on an antigenic change, the wild strain should differ
from all aggregateless ones, and it would thus be profitable to try to