212
F. C. STEWARD AND Η. Y. MOHAN
RAM
ment it is now well known that protein and other syntheses occur (cf.
Steward and Thompson, 1954 and references there cited), but these are
more readily interpretable as part of the train of growth events set up by
the auxin than as the primary seat of the auxin effect.
The cell wall, because of its ease of extension, has been, ever since the
work of Heyn (1931) on plastic versus elastic extension of the wall, a
favoured site for the effects induced by auxins. The unidirectional
elongation of cell walls in root apices is supposed to occur in two stages
(Burström, 1957). The first stage is a plastic extension of the cell wall
induced by auxin, but inhibited by coumarin, and this is independent
of calcium. The second phase is growth by intussusception wherein new
wall material is filled in between the loosened microfibrils. This latter
stage is said to be auxin inhibited, has a strong calcium requirement, and
is uninhibited by coumarin. Thus, according to Burström (1957), the
growth inhibition by auxin in a root is not on the plastic stretching
(which can amount only to a part of the total elongation) but on the
second phase, involving the incorporation of new building material into
the wall. Cell wall loosening effects, attributable to auxin-induced
methylation of pectins, as components of the wall, have been advocated
by Bennet-Clark (1956), Ordin, Cleland and Bonner (1957) and Glasziou
(1957). The hypothesis that polysaccharide synthesis may be so stimulated by auxin that the wall 'grows' has been experimentally disproved
by Wightman (1955, cited from Bennet-Clark, 1956), who showed that
considerable extension in the wheat coleoptiles could occur without
appreciable increase in cellulose synthesis. However, there is still no
generally accepted reaction in which the natural or the numerous
synthetic auxins are known to intervene with determining effects upon
the structure, elasticity, or plasticity of the cell wall. If the main seat
of the auxin effect is in the cell wall, it would need to be interpreted at
the submicroscopic level. Thus, in primary walls, the auxin could loosen
the tangled weft of randomly arranged fibrils, whereas in secondary walls
of elongating cells, it would need to modify the spiral arrangement of cellulose that normally obtains in such situations. There is, however, no generally accepted interpretation which covers all these different situations.
It is still most probable that the auxins, and the gibberellins, the
effects of which are of the same general kind, must intervene in some
essential metabolic reaction or process which is concerned with growth—
growth in which cell enlargement predominates. Similarly, other substances—the kinins of Skoog et al.—must intervene in other processes
which are concerned with growth primarily by cell division (cf. Sect. II
A 1 below). Even though the mode of action of these natural and synthetic growth-regulatory substances cannot yet be satisfactorily explained, their effects are demonstrable.
F. C. STEWARD AND Η. Y. MOHAN
RAM
ment it is now well known that protein and other syntheses occur (cf.
Steward and Thompson, 1954 and references there cited), but these are
more readily interpretable as part of the train of growth events set up by
the auxin than as the primary seat of the auxin effect.
The cell wall, because of its ease of extension, has been, ever since the
work of Heyn (1931) on plastic versus elastic extension of the wall, a
favoured site for the effects induced by auxins. The unidirectional
elongation of cell walls in root apices is supposed to occur in two stages
(Burström, 1957). The first stage is a plastic extension of the cell wall
induced by auxin, but inhibited by coumarin, and this is independent
of calcium. The second phase is growth by intussusception wherein new
wall material is filled in between the loosened microfibrils. This latter
stage is said to be auxin inhibited, has a strong calcium requirement, and
is uninhibited by coumarin. Thus, according to Burström (1957), the
growth inhibition by auxin in a root is not on the plastic stretching
(which can amount only to a part of the total elongation) but on the
second phase, involving the incorporation of new building material into
the wall. Cell wall loosening effects, attributable to auxin-induced
methylation of pectins, as components of the wall, have been advocated
by Bennet-Clark (1956), Ordin, Cleland and Bonner (1957) and Glasziou
(1957). The hypothesis that polysaccharide synthesis may be so stimulated by auxin that the wall 'grows' has been experimentally disproved
by Wightman (1955, cited from Bennet-Clark, 1956), who showed that
considerable extension in the wheat coleoptiles could occur without
appreciable increase in cellulose synthesis. However, there is still no
generally accepted reaction in which the natural or the numerous
synthetic auxins are known to intervene with determining effects upon
the structure, elasticity, or plasticity of the cell wall. If the main seat
of the auxin effect is in the cell wall, it would need to be interpreted at
the submicroscopic level. Thus, in primary walls, the auxin could loosen
the tangled weft of randomly arranged fibrils, whereas in secondary walls
of elongating cells, it would need to modify the spiral arrangement of cellulose that normally obtains in such situations. There is, however, no generally accepted interpretation which covers all these different situations.
It is still most probable that the auxins, and the gibberellins, the
effects of which are of the same general kind, must intervene in some
essential metabolic reaction or process which is concerned with growth—
growth in which cell enlargement predominates. Similarly, other substances—the kinins of Skoog et al.—must intervene in other processes
which are concerned with growth primarily by cell division (cf. Sect. II
A 1 below). Even though the mode of action of these natural and synthetic growth-regulatory substances cannot yet be satisfactorily explained, their effects are demonstrable.