194 CONTROL MECHANISMS IN CELLULAR PROCESSES 



out chaniiing the total number of bonds. This would mean that 

 stretching is controlled by the breaking of ])onds by a chemical 

 process ( methylation ) rather than by forcible physical deformation 

 ( "pulling" bonds apart ) ; the former process could not be considered 

 a passive plastic stretching in the sense that the latter is. If the 

 total number of cross-links were, as indicated, no different in the 

 presence and absence of auxin, the physical "plasticity" of the cell 

 wall, if it does have such a property, should be no different. The 

 present author (Rav, 1960) has called this type of possible growth 

 mechanism a "molecular mosaic," because it is somewhat analogous, 

 at the molecular level, to the "mosaic growth" proposed by Frey- 

 Wyssling and Stecher (1951), which was supposed to occur step- 

 wise by loosening in localized areas of the cell wall, while the wall 

 structure as a whole remained rigid. (The "mosaic growth" pro- 

 posal itself has not attracted wide support, since the electron micro- 

 graphs on which it was based can be interpreted quite differently. ) 



The pectin cross-linkage hypothesis thus calls one's attention to 

 two biophysically different tvpes of possible growth mechanism 

 which there has been some tendencv to confuse under the notion of 

 "plasticitv." The question of which tvpe of mechanism, if either, is 

 actually involved in growth appears to be a fundamental and gen- 

 eral one irrespective of whether the pectin cross-linkage hypothesis 

 itself is correct, and we shall return to it subsequently. 



The pectin hypothesis seems to be encountering further difficul- 

 ties. Jansen et al. (1960) reported that the hot-water-soluble pectin 

 is almost fully esterified, whereas the residual insoluble polyuronides 

 ( "protopectin" ) , comprising more than 80 per cent of the total cell 

 wall uronic acid, are onlv about 30 per cent esterified. So it appears 

 that the number of possible double salt cross-links in that fraction 

 in which lAA does promote methylation (the water-soluble) is a 

 very minor proportion, less than 3 per cent, of the total, and it is 

 rather hard to see how these few cross-links could be the critical ones 

 to cell wall rigidity. Also, from the fact that the hot-water-soluble 

 material is the most easily removed, hence least strongly bonded cell 

 wall constituent, it would seem unlikey that bonding involving the 

 hot-water-soluble fraction could be of critical importance in the 

 strength of the cell wall. It seems entirely possible that the inhibi- 

 tion of growth by Ca++ is caused by an "artificial" rigidification of 

 the cell wall through setting up double salt cross-links which, in the 



