PLANT GROWTH 



to 6.2% after 24 h. (based on initial dry weight). Furthermore, and most important, 

 arsenite and other inhibitors prevent this decrease in fat. Correspondingly, they 

 raise the RQ, back to i .0, or even above it. It was deduced that the major substrate 

 for elongation (after the first few h.) is fat, that about equal quantities of fat and 

 sugar are oxidized, and that some of the fat is continuously converted to sugar via 

 processes poisoned by arsenite, fluoride or iodoacetate. Since these metabolic 

 poisons can all act on several enzymes it is not surprising that they would all 

 prevent the fat-sugar conversion, which involves combination with coenzyme 

 A(requiring ATP), degradation to 2-carbon fragments, formation of pyruvate 

 and thence of triose, followed by condensation to hexose. 



In roots fat may also be a major metabolite, though perhaps not for growth. 

 After wheat roots are cut off, the respiration decreases for some h. and simultane- 

 ously the RQ_ falls from a little above i to 0.7-0.8. Added glucose prevents the fall. 

 The RQ, in the elongating zone, however, remains close to i for at least 6 h., 

 indicating that carbohydrates are, at least at first, the main substrate for elongation 

 (Karlsson and Eliasson, 1955). The values 0.7-0.8 strongly indicate fat oxidation 

 in the root as a whole but the authors do not draw this conclusion. The respiratory 

 rate in the elongating zone is almost double that in the zone of cell division or that 

 in the more basal maturing zones (Kopp, 1948; Goddard and Meeuse, 1950). 



{Hi) Formation of enzymes and proteins. In many isolated tissues enzymes are formed 

 during growth. Isolated sections of roots elongating in a simple solution (Robinson 

 and Brown, 1954) synthesized a slight amount of phosphatase, but lost invertase 

 during elongation. However, since their growth is not promoted by auxin these 

 root sections cannot be used to determine the effect of auxin on enzyme activity. 

 The change in the terminal oxidase of potato slices, mentioned above, is another 

 example but although this follows cell enlargement, it appears not to be connected 

 with auxin action since the change occurs in water as well. Although auxin has 

 not yet been proven to exert any recognizable effect on an enzyme system in vitro, 

 there are at least three reports that after auxin has acted on a tissue, the enzyme 

 content of the tissue has increased. 



The first of these concerned ascorbic acid oxidase, which was foiuid to be very 

 greatly increased in tobacco pith tissue after it had been caused to grow by lAA 

 (Newcomb, 1951). The increase was of the order of nearly 400% and reached a 

 maximum after 14 days. (The growth of this tissue is by no means pure cell 

 enlargement, since numerous mitoses, including highly polyploid ones, have been 

 reported in it [Skoog, 1953])- The ascorbic oxidase was of a peculiar kind, being 

 centrifuged down at low speeds with the cell-wall fragments. Most, but not all, 

 workers with other tissues have found this enzyme to be soluble. 



The connection with the cell-wall was still stronger in the second instance, when 

 Bryan and Newcomb (1954) found pectin methylesterase increased in the same 

 tissue after growth in lAA. Since pectin esters hydrolyze very readily under a 

 variety of conditions, the significance of the enzyme is not wholly clear, though 

 its relation to cell-wall metabolism is very suggestive. Indeed this observation led 

 to a theory of the mode of auxin action, centering on the properties of the cell 

 wall (see section VIj, p. 793). 



The third instance involves a quite unrelated enzyme, namely peroxidase 



