GROWTH SUBSTANCES-RED LIGHT INTERACTIONS 193 



represented as acting only on endogenous growth. Note that lAA is 

 also represented as inhibiting endogenous growth, an effect easily 

 demonstrated with sections taken very close to the apex (Purves and 

 Hillman, 1958). This interaction provides an explanation for the fact 

 that high lAA levels suppress both the red and FR response (Fig. 6). 



If a sufficiently high lAA level, while causing elongation on its own, 

 completely represses that portion of the endogenous growth also 

 inhibitable by red light, no red inhibition will be detected in its pres- 

 ence. This interpretation is strengthened by the fact that, for sections 

 from dark-grown plants, the concentration of lAA required to prevent 

 red inhibition is supraoptimal, so that it is evident that an inhibition of 

 some sort is occurring. On the assumption that all endogenous growth 

 is identical with lAA-induced growth, this inhibition would simply be 

 due to excess lAA in a single system, but only on this assumption. It 

 is equally likely that the lAA response curve of sections from dark- 

 grown plants is the resultant of a promoting action on one system 

 (lAA-induced growth) and an inhibiting action on another (endoge- 

 nous growth). Significantly, the prevention of red inhibition by high 

 lAA is not a true reversal, since elongation is not restored to the peak 

 given by IQ-^M lAA in the absence of red. A similar observation was 

 made for the A vena first internode by Schneider (1941, Fig. 12). 



The suppression of FR promotion by high lAA can be similarly 

 interpreted. An alternative explanation is that elongation at high lAA 

 is limited here by other factors, such as energy-rich substrate or 

 structural materials, but several experiments have shown that GA can 

 still increase elongation at high lAA levels, so that this seems unlikely. 



In terms of this scheme, then, sections from dark-grown plants are 

 inhibited by red light because an endogenous growth component is 

 inhibited; sections from red-grown plants are not inhibited by red 

 because this component no longer contributes to elongation unless it 

 is de-inhibited by FR; this same component is also inhibited by suffi- 

 ciently high levels of lAA. The results of Galston and Baker (1953) 

 may perhaps be explained on this basis. If the apparently lower lAA 

 optimum of sections from dark-grown plants is due simply to an inhibi- 

 tion of endogenous growth by lAA, and if this inhibition is already 

 "saturated" in sections of red-grown plants, then elongation will be 

 promoted in the latter by considerably higher lAA levels. 



The position of kinetin in Fig. 7 is easily explained. It inhibits 



