384 P. M. Ray 



which would be involved in the mechanism discussed here. We shall 

 call the active process of bond breaking pictured here the molecular 

 mosaic growth mechanism in contrast to the passive plastic type of 

 deformation discussed earlier. The basic difference between them is, 

 in sum, whether it is the force of turgor or an act of the cell which 

 breaks the bonds as the cell grows. 



These contrasting mechanisms provide some interesting problems. 

 Many of the characteristics of the growth process could result from 

 operation of either mechanism — this was illustrated above by the 

 dependence upon tmgor pressure. It is important to note that in 

 the measurement of cell wall plasticity (7) one may be dealing ^vith 

 either mechanism of enlargement and therefore not necessarily ^\•ith 

 strict plasticity at all. On the other hand, a clearer view of the prob- 

 lem may suggest experimental approaches useful in revealing the 

 actual mechanics of cell enlargement. As indicated above, one dis- 

 tinction can be made between the number of bonds present and the 

 rate at which bonds are broken. It should be emphasized again that 

 these bonds may not in fact be calcium salt bridges between uronide 

 chains; the distinction will apply to whatever critical bonds are actu- 

 ally involved in cell enlargement. 



It is not, of course, necessarily the case that cell growth can be 

 described by any single type of molecular event, and it seems possible 

 that both plastic and molecular mosaic types of extension may con- 

 tribute to over-all growth. This does not diminish the importance of 

 the distinction. It also can serve as a starting point for considering 

 more complex forms of bonding which may be involved in cell 

 growth. One example will be given: Suppose that the basis for rigid- 

 ity of the cell wall matrix is interlocking of polysaccharide chains 

 which run randomly and occasionally happen to be caught together 

 in loops, as in a knitted fabric. Extension of such a structure can be 

 brought about only by severing one or both chains in the vicinity of 

 a loop (a molecular mosaic, since splitting of the covalent bond pre- 

 sumably would occur by a metabolic process). Expansion of the 

 structure would soon result in other chains, which were previously 

 not in contact, becoming entangled, and thus assuming the stress on 

 the wall and restoring rigidity. In this model, new forces tending to 

 stillen the wall arise automatically upon extension, and auxin treat- 

 ment of cells under no turgor could result in a subsequent limited 

 extension of the wall, as has been observed in some experiments (2, 8). 



SUMMARY 



There are a number of problems in the biophysics of cell wall 

 growth concealed under the vague concej)t of plasticity. The possible 



