6. PHOTOTROPISM AND PHOTOTAXIS
299
that 100 meter-candles for five hours (= 1.8 X 10
6 MCS) was "not yet
effective" in causing growth inhibition. (The tip response is optimal at
about 200 MCS; see Fig. 2). Unless it can be shown that auxin transport inhibitors are photolytically formed with much greater efficiency in
the tip than elsewhere, we must look for some other and more powerful
type of amplification to explain the tip response.*
The simplest expedient is the broad assumption that the activity of
an enzyme in the auxin production-transport system is changed by light.
A possible parallel may be found in the effect of ionizing radiations on
an auxin-forming enzyme (150). In phototropism the light must be absorbed by a pigment, either intimately associated with the enzyme or
capable of direct interaction with it. We have already seen that the
decreasing phase of the response curve can be attributed to lightsaturation. As in the "base response" mechanism, we must then assume
a back reaction, regenerating the pigment (or enzyme), to account for
the large tip curvatures which develop under continuous low-intensity
exposures.
An explanation for negative curvatures is called for. Like the positive
tip curvatures, the ultimate effector of these is an auxin redistribution
(cf. Table IV). Therefore the same pigment system is probably involved.
The most probable assumption is that the negative curvatures are due
to an irreversible bleaching of the photoreceptor pigment at sufficiently
high intensities, before reaction with the enzyme. This would simultaneously explain the intensity requirement for negative curvatures and
the fact that smaller curvatures are obtained with continuous exposures
to such intensities (cf. Table I).
A quite different explanation has been advanced by Meyer and Pohl
(148) according to which light converts IAA to inhibitory breakdown
products which are themselves photosensitive and give rise to compounds which are not inhibitory. Unfortunately one of the best established intermediates (151) in the photolytic sequence is indole-3-aldehyde, which is not in the least photosensitive even in presence of riboflavin. However, it is readily converted by Schardinger enzyme, which
is known to be present in the plant, to indolecarboxylic acid, which is
again photosensitive and breaks down to anthranilic acid and eventually
to oxalic and formic acids and glycine (see Scheme II).
* Note added in proof: Since the above was written, another example of this
(very common) lack of appreciation of the low light dosages effective in phototropism has come to hand in the paper of Fang et al. (149a) who found a 20%
increase in the amount of IAA decomposed in corn shoots after exposure to about
13 million MCS, and ascribe significance to this for the explanation of phototropism.
299
that 100 meter-candles for five hours (= 1.8 X 10
6 MCS) was "not yet
effective" in causing growth inhibition. (The tip response is optimal at
about 200 MCS; see Fig. 2). Unless it can be shown that auxin transport inhibitors are photolytically formed with much greater efficiency in
the tip than elsewhere, we must look for some other and more powerful
type of amplification to explain the tip response.*
The simplest expedient is the broad assumption that the activity of
an enzyme in the auxin production-transport system is changed by light.
A possible parallel may be found in the effect of ionizing radiations on
an auxin-forming enzyme (150). In phototropism the light must be absorbed by a pigment, either intimately associated with the enzyme or
capable of direct interaction with it. We have already seen that the
decreasing phase of the response curve can be attributed to lightsaturation. As in the "base response" mechanism, we must then assume
a back reaction, regenerating the pigment (or enzyme), to account for
the large tip curvatures which develop under continuous low-intensity
exposures.
An explanation for negative curvatures is called for. Like the positive
tip curvatures, the ultimate effector of these is an auxin redistribution
(cf. Table IV). Therefore the same pigment system is probably involved.
The most probable assumption is that the negative curvatures are due
to an irreversible bleaching of the photoreceptor pigment at sufficiently
high intensities, before reaction with the enzyme. This would simultaneously explain the intensity requirement for negative curvatures and
the fact that smaller curvatures are obtained with continuous exposures
to such intensities (cf. Table I).
A quite different explanation has been advanced by Meyer and Pohl
(148) according to which light converts IAA to inhibitory breakdown
products which are themselves photosensitive and give rise to compounds which are not inhibitory. Unfortunately one of the best established intermediates (151) in the photolytic sequence is indole-3-aldehyde, which is not in the least photosensitive even in presence of riboflavin. However, it is readily converted by Schardinger enzyme, which
is known to be present in the plant, to indolecarboxylic acid, which is
again photosensitive and breaks down to anthranilic acid and eventually
to oxalic and formic acids and glycine (see Scheme II).
* Note added in proof: Since the above was written, another example of this
(very common) lack of appreciation of the low light dosages effective in phototropism has come to hand in the paper of Fang et al. (149a) who found a 20%
increase in the amount of IAA decomposed in corn shoots after exposure to about
13 million MCS, and ascribe significance to this for the explanation of phototropism.