794 PLANT GROWTH lO 



molecule of auxin caused the deposition of more than one "molecule" of cellulose 

 and indeed that not enough auxin was taken up to form a monomolecular 

 layer over the surface of the newly-formed cell walls. Work on the physical and 

 mechanical properties of the walls of growing organs, notably by Heyn and by 

 Soding, did show that the plastic extensibility of the walls was increased by auxin 

 action (see Went and Thimann, 1937; Heyn, 1940, and Audus, 1949, for reviews). 

 This led to the general concept that auxin causes cell enlargement by loosening 

 the rigid structure of the wall, perhaps by enabling the cellulose micelles to sepa- 

 rate from one another. Whether insertion or intussusception of new micelles 

 between the old ones was a necessary accompaniment, or whether no more than 

 a kind of passive stretching was involved, remained uncertain. From experiments 

 with roots, Burstrom (1953a, c, 1954) came later to the view that both intussuscep- 

 tion and stretching occvirred, but in sequence, pure stretching constituting the 

 first phase and wall deposition the second. Auxin was considered to promote the 

 first phase in all concentrations but to inhibit the second at levels above io~''M, 

 so that total growth of the root became inhibited in all but the very lowest concen- 

 trations. 



These actions are envisaged as essentially physical. Other "physical" views 

 have been put forward both before and subsequently. For example, Ruge in 1937 

 proposed that auxin becomes concentrated in the cell wall, increasing the acidity 

 there and consequently (both by its acidity and by the specific effects of its anion) 

 making the intermicellar colloids swell. Northen (1942, 1946 and other papers 

 there cited) found that natural and synthetic auxins decreased the viscosity of the 

 cytoplasm, as measured by high-speed centrifugation. This led him to the view 

 that auxin causes the dissociation of complex proteins. As a result the viscosity 

 would decrease, the protoplasmic swelling pressure would increase, and cell 

 enlargement was considered to be a natural consequence. It was even suggested 

 that the protein dissociation might liberate free -SH groups, which certainly 

 participate in growth (Sect. Vlf). Northen's observations of changes in viscosity 

 may be another aspect of the increase in protoplasmic streaming rate caused by 

 auxin (see below). Another physical view was based on the relation between 

 chemical structure of the auxins and their growth-promoting activity and is largely 

 due to Veldstra (see Veldstra, 1953, and Muir and Hansch, 1955, for reviews). The 

 requirement for a ring and for one or more double bonds in it was ascribed by 

 Veldstra to the necessity for the molecule to be adsorbed on a specific surface. The 

 substitution of CI atoms in the ring was supposed to enhance activity by increasing 

 the lipophilic character of the ring and thus increasing its adsorption on to a lipoid 

 phase. The well-known auxin activity of the c/i'-forms of cinnamic, /^-methoxy 

 cinnamic, a-naphthaleneacrylic and tetralideneacetic acids, and the inactivity of 

 their /ra«j^-isomers (p. 765), was ascribed to the necessity of holding the dipole of 

 the carboxyl group out of the plane of the ring. Models show that this does occur 

 readily in at least some of the cis-ac'ids. Thus the auxin-molecule was considered 

 to be adsorbed on a cell boundary, its ring in the lipoid phase of the membrane 

 and its carboxyl group projecting out into the acjueous phase of the cytoplasm 

 (see Fig. 10) In this state, Veldstra believed, the molecule would strongly influence 

 the membrane potentials and by "opening" the tight packing of the membrane. 



