142
LUISE STANGE
centres of small cells. In the concentrations 10
- 5
and 5 x 10~
5
g/ml only
callus-like outgrowth was produced. Cytological examination revealed
that, although in all non-toxic concentrations of IAA nuclear division
occurred, the progression of divisions was much delayed. After the first
nuclear divisions the daughter nuclei were scattered over the whole
enlarging cell. Normally, they lie close together in one part of the mother
cell forming a centre of small meristematic cells. In isolated tissue the
formation of rhizoids was greatly increased under the influence of IAA
in the concentrations 10
- 8
to 10
- e
g/ml. IAA did not cause rhizoid
formation after isolation of individual cells or small groups of cells by
plasmolysis. I t is assumed that IAA influences the correlations between
the cells of isolated tissue, inhibiting the formation of centres of small
meristematic cells. But no prevention of embryonization was observed.
No inhibition of regeneration was found after treatment of isolated
leaves of Splachmim with IAA over a broad concentration range
(MacQuarrie and von Maltzahn, 1959). Inhibition was observed only at
high concentrations (10
- 5
g/ml), but in this case the material was visibly
damaged. The effect of IAA was tested also on protonema regeneration
from the basal part of the gametophore stem, which occurs after decapitation of the gametophore apex. (Protonema formation in this
region occurs to some extent also in intact plants.) Attempts were made
to substitute the effect of the gametophore apex by IAA. The results
show (Table I) that only non-physiologically high concentrations of
10
- 3
g/ml IAA could replace the effect of the apex. This concentration
is even higher than the concentration necessary for replacement of the
apex in inhibition of lateral buds (10~
4
g/ml, cf. Section II). Since decapitation of the gametophore resulted in basal protonema regeneration
and in lateral bud reactivation and since application of IAA to the tip of
decapitated plants inhibited both processes, the question arises whether
both processes are governed by the same IAA controlled mechanism. I t
was therefore tested, as in the experiments on lateral bud reactivation
(cf. Section II), whether an interaction between auxin and kinetin
exists for protonematal regeneration from the base of the gametophore
(von Maltzahn, 1959). While kinetin had a strong antagonistic effect on
the action of IAA in lateral bud reactivation, it did not seem to have
any effect in counteracting IAA in basal protonema regeneration
(Table I). Kinetin must reach the base of the gametophore, since it is
apparent from this Table that kinetin counteracts the inhibitory effect
of IAA also for the most basal buds close to the site of basal regeneration.
These results suggest that the mechanisms of correlations inhibiting
lateral bud reactivation and basal protonema regeneration in the
presence of the apical region of the gametophore are different.
Further experiments were carried out with Splachnum to study the
LUISE STANGE
centres of small cells. In the concentrations 10
- 5
and 5 x 10~
5
g/ml only
callus-like outgrowth was produced. Cytological examination revealed
that, although in all non-toxic concentrations of IAA nuclear division
occurred, the progression of divisions was much delayed. After the first
nuclear divisions the daughter nuclei were scattered over the whole
enlarging cell. Normally, they lie close together in one part of the mother
cell forming a centre of small meristematic cells. In isolated tissue the
formation of rhizoids was greatly increased under the influence of IAA
in the concentrations 10
- 8
to 10
- e
g/ml. IAA did not cause rhizoid
formation after isolation of individual cells or small groups of cells by
plasmolysis. I t is assumed that IAA influences the correlations between
the cells of isolated tissue, inhibiting the formation of centres of small
meristematic cells. But no prevention of embryonization was observed.
No inhibition of regeneration was found after treatment of isolated
leaves of Splachmim with IAA over a broad concentration range
(MacQuarrie and von Maltzahn, 1959). Inhibition was observed only at
high concentrations (10
- 5
g/ml), but in this case the material was visibly
damaged. The effect of IAA was tested also on protonema regeneration
from the basal part of the gametophore stem, which occurs after decapitation of the gametophore apex. (Protonema formation in this
region occurs to some extent also in intact plants.) Attempts were made
to substitute the effect of the gametophore apex by IAA. The results
show (Table I) that only non-physiologically high concentrations of
10
- 3
g/ml IAA could replace the effect of the apex. This concentration
is even higher than the concentration necessary for replacement of the
apex in inhibition of lateral buds (10~
4
g/ml, cf. Section II). Since decapitation of the gametophore resulted in basal protonema regeneration
and in lateral bud reactivation and since application of IAA to the tip of
decapitated plants inhibited both processes, the question arises whether
both processes are governed by the same IAA controlled mechanism. I t
was therefore tested, as in the experiments on lateral bud reactivation
(cf. Section II), whether an interaction between auxin and kinetin
exists for protonematal regeneration from the base of the gametophore
(von Maltzahn, 1959). While kinetin had a strong antagonistic effect on
the action of IAA in lateral bud reactivation, it did not seem to have
any effect in counteracting IAA in basal protonema regeneration
(Table I). Kinetin must reach the base of the gametophore, since it is
apparent from this Table that kinetin counteracts the inhibitory effect
of IAA also for the most basal buds close to the site of basal regeneration.
These results suggest that the mechanisms of correlations inhibiting
lateral bud reactivation and basal protonema regeneration in the
presence of the apical region of the gametophore are different.
Further experiments were carried out with Splachnum to study the