HORMONAL REGULATION OF PLANT CELL GROWTH 193 



wliicli could cross-link galacturoiiic acid residues of different pectin 

 molecules and might thus be expected to stiffen the cell wall, in- 

 hibiting growth. In pectin some of the carboxyl groups arc esteri- 

 fied witli methanol and hence cannot form salts or cross-links. These 

 authors envisioned that the action of auxin could be to promote the 

 metabolic "meth\ lation" of pectin carboxyl groups and, by reducing 

 the number of possible cross-links, increase the "plasticity" of the cell 

 wall. 



Ordin, Cleland, and Bonner (1955, 1957) reported that auxin 

 did promote the incorporation of C" from methyl-labeled methi- 

 onine (a suitable methyl donor) into ester groups of the hot water 

 soluble pectin of oat coleoptile cell walls (although it did not pro- 

 mote the much larger incorporation into insoluble "protopectin" ) . 

 This effect has been found also in corn coleoptiles— but not in first 

 internodes of corn seedlings, the growth of which is promoted by 

 auxin (Cleland, 1960). These workers have felt that this effect of 

 auxin could be directly responsible for its promotion of growth. 

 Adamson and Adamson ( 1958 ) , who gave a succinct description of 

 the pectin hvpothesis, found support for it in effects on cell wall 

 "plasticity" caused by auxin at 3° C and in the absence of O2, which 

 they felt were consistent with the idea that auxin increases the 

 methyl ester content of cell wall pectin by inhibiting the hydrolysis 

 of methyl ester groups by pectin methylesterase. 



The pectin cross-linkage hypothesis is about the only specific 

 chemical explanation which has been advanced as to how auxin can 

 affect the "plasticity" of the cell wall, and it attractively explains 

 why "plasticity," hence growth, should depend upon metabolism. 



Jansen et al. ( 1960 ) analyzed oat coleoptile cell walls in respect 

 to uronic acid residues and methyl ester groups. They found no 

 change in the absolute amounts of either of these in the presence 

 of auxin (although auxin promotion of incorporation of labeled 

 methyl into pectin ester was confirmed). Thus it seems necessary 

 to give up the idea that an increase in plasticity could result from 

 a decrease in the number of pectin double salt cross-links in the 

 presence of auxin; Bennet-Clark has also reached this conclusion 

 (see Galston and Purves, 1960). It was thought possible that in- 

 creased ft/rnouer— increased rate of formation and removal of methyl 

 ester groups— could be occurring. If this were to cause increased 

 "plasticity," what must be contemplated is that auxin increases the 

 rate of wall stretching by increasing the rate of bond breaking, with- 



