328 y. Bonner 



in the plasticity of the thick oblique walls, and the second is genera- 

 tion of the necessary osmotic pressure to maintain or increase turgor. 



Both these processes only occur after the geotropic stimulus. I 

 would not like to state that we have "hormones," one producing plas- 

 ticity and another generating high osmotic pressure until a better 

 and more extensive survey of growth substances separated by chroma- 

 tography has been completed. (I remember my first chief's advice: 

 "Beware of the devil because the devil always sends positive results 

 first!") 



The point I want to make is that in almost all of our discussion 

 about auxin action and about the activity of substituted phenoxy- 

 acetic acids, indoles, and so forth, we assume that because our test 

 process is an expansion in length, it is always the same molecular 

 process that is involved in bringing about the expansion in length. 

 In the node it is quite clear that there are at least two (possibly more) 

 completely separate processes: one is wall softening and the other is 

 build-up of osmotic pressure. In the node this osmotic pressure is quite 

 certainly due to entry of or production of sugars in the lo^ver-side cells. 

 The data will be published soon. 



In corn mesocotyls, however, we find that the sugar concentration 

 decreases, whereas that of potassium ions increases very markedly on 

 the lower side. 



Growth initiated by so-called hormones involves this complex of 

 processes and may thus really require a complex of hormones for 

 its completion. The process initiated by a synthetic substance like 2,4-D 

 may be a different process from any of those initiated by the natural 

 gravitational hormone or by lAA, though each of these possibly dif- 

 ferent processes provides the same end result — namely cell extension. 



I would like to refer to the views put forward by me earlier. Indole- 

 3-acetic acid does affect wall extensibility, and I thought cross link- 

 ages between polysaccharide molecules, especially pectins, the most 

 likely point of attack, and that the mechanism was through control of 

 the methylation of pectin. This view was based on preliminary 

 analyses of the methoxyl content, and we thought also that we had 

 demonstrated a transmethylation accelerated by lAA. 



Later work in our laboratory has shown that there is no difference 

 in the degree of methylation of wall pectin in stems and mesocotyls 

 as a consequence of increased extensibility caused by lAA. We had, 

 of course, thought that increased methylation and consequent de- 

 creased calcium in the wall was the cause of increased extensibility. 



W^e still have to find a molecular mechanism to explain this in- 

 creased wall extensibility, and I now no longer favor the pectin- 

 methylation hypothesis. 



