Stimulation of Auxin Action by Lipides 425 



vanced the hypothesis that the effect of the lipides is due to their 

 activation of the cytochrome system leading to a greater availability 

 of energy for growth (17). The results which have been outlined 

 above bear an amazing similarity to the data obtained by workers 

 with animal systems of isooctane-extracted cell particles (5, 7, 23). 

 In these systems the cytochrome activity of the particles can be re- 

 stored by a number of lipide compounds which apparently facilitate 

 the action of cytochrome-c reductase. Table 4 gives the results of a 

 comparison of a number of compounds which have been tested in 

 both the pea system and with the isooctane-extracted particulates. 

 Of the 19 compounds only 4 show activity in one system and not in 

 the other, and in each of these cases the activity that was observed 

 was submaximal. The analogy probably does not hold in another 

 case, since in a few tests with coenzyme Qio," a lipide-soluble quinone 

 which is found in plants (4) and which acts on mitochondrial electron 

 transport, no convincing effect could be noted in our system. Further- 

 more, the inhibition of section growth caused by antimycin A was 

 not reversed by vitamin Kj, but an irreversible effect of this inhibitor 

 is also shown by some particulate systems (5). 



Further support to the idea that the respiratory system is involved 

 is given by the data of Figure 2 which show that both methyl myristate 

 and vitamin E increase the respiration of the sections above the 

 values obtained in auxin plus GA3 alone. Although this promotion 

 is not large, it is comparable to that produced by auxin over the con- 

 trols in basal medium, which would be expected from the fact that 

 the growth increments in each case are roughly the same. 



Obviously, evidence of this kind cannot conclusively implicate 

 the cytochromes. However, the work of Hackett and Schneiderman 

 (11) makes it clear that the auxin-induced growth of pea sections is 

 entirely mediated by cytochrome oxidase. Since this is the case, a 

 limitation of growth imposed by a deficiency in cytochrome-c reduc- 

 tion is all the more plausible. Direct observations of cytochrome-c 

 activation will have to be made to prove this hypothesis. This may 

 be difficult without disruption of the tissue and a consequent loss of 

 the linkage to cell elongation. 



Additional speculation along these lines might also be made for 

 the case of the growth-promoting effect of cobalt which requires 

 sucrose (14,22). The lipide effect is considerably accentuated by 

 sucrose (18); cobalt has a smaller promotive role (19). In yeast, co- 

 balt can induce respiratory deficiencies, probably due to an effect on 



Kindly supplied by Dr. F. L. Crane. 



