324 ]. Bonner 



ROLE OF PECTIN ESTERASE 



There has been extensive discussion of the possible role of pectin 

 esterase in auxin-induced growth. Glasziou (13) and Glasziou and In- 

 glis (14) in particular have suggested, on the basis of experiments 

 with tobacco pith and Jerusalem artichoke tuber tissue, that auxins 

 function by binding and thus inactivating pectin esterase. Avena 

 coleoptile sections do indeed contain readily detectable amounts of 

 pectin esterase (Jansen et ah, 17), essentially all of which is bound to 

 cell wall. lAA is, however, without direct effect either on this binding 

 or on the activity of the enzyme in Avena coleoptile sections (17). It 

 has already been shown above that the role of lAA in pectic metabo- 

 lism lies in an earlier step than that mediated by pectin esterase. 



SUMMARY 



There appear to be two general approaches to the study of auxin 

 action. The first is to determine with what material added auxin in- 

 teracts within the cell, find out what the interaction product does, and 

 so step by step, trace the sequence by which cell wall softening is id- 

 timately brought about. The second approach is to start at the op- 

 posite end of the chain, namely with the final result of wall softening, 

 discover what chemical changes bring about this effect, and step by 

 step trace the sequence forward to the initial interaction of auxin 

 with plant. Both approaches have been used but we are as yet far 

 from linking them. On the one hand, it appears that auxin does in- 

 teract within the plant with a specific receptor entity and that this 

 interaction involves two point-combination of auxin and receptor 

 (Bonner and Foster, 8). Identification of the auxin-receptor complex 

 by the use of labeled auxin has so far failed, and we conclude only 

 that the complex is present in the plant tissue at very low concentra- 

 tion, of the order of 1 part in 100,000,000 or less. The approach from 

 analysis of cell extension itself has, however, been, as shown above, 

 appreciably fruitful. It is clear that auxin-induced growth is the re- 

 sult of auxin-induced cell wall softening and that this is in turn as- 

 sociated with auxin-induced alteration in the synthesis of cell wall 

 pectic material. Elucidation of the way in which auxin influences pec- 

 tin synthesis requires that the enzymology of pectic synthesis first be 

 understood, which it is not. This then is the present state of the study 

 of the mechanism of auxin action in the Aveyia coleoptile section. 



The facts presented above are numerous and complex. It may be 

 j)crhaps of passing value to summarize them in terms of a model 

 which, although it may very well be incorrect, will nonetheless serve 

 to help us remember some of the facts. This model, which concerns 

 the parenchymatous cells of coleoptile section and disregards the epi- 



