Mechanics of Auxin-induced Growth 325 



dermal cells (which serve merely to slow the growth of the section) 

 (Bonner, 5), starts with the observations of Miihlethaler (19) and of 

 Wardrop (27, 28) that dining elongation of coleoptile parenchyma 

 cell walls the constituent cellulose microfibrils are steadily separated 

 from one another and dispersed from their initially transverse orien- 

 tation. In addition, however, new, transversely oriented microfibrils 

 are steadily added on the inner surface of the wall. Evidently as the 

 wall is stretched during elongation, the microfibrils are pulled apart 

 into a more disperse network and reoriented in the direction of 

 stretch just as in inanimate model systems. We may imagine then that 

 as the wall is stretched, as junction after junction yields and breaks 

 under tension, it becomes progressively weaker. The mechanical 

 strength of the wall is maintained only because of the constant addi- 

 tion of new material to its inner surface. The present model then 

 assumes that the mechanical strength of the cell wall is primarily 

 determined by the most recently deposited material. 



Further questions with which the model concerns itself are: What 

 properties of the wall determine how tightly the cellulose microfibrils 

 are linked together? What determines how readily they may be pulled 

 apart? The model nominates the pectic molecules for this function. 

 The long random coils of pectic material intertwine the microfibrils 

 as fungal hyphae intertwine the clay particles in a soil, binding the 

 whole into an interconnected network. And in this function long 

 pectic chains will evidently be more effective than short ones. The 

 addition of auxin to the tissue encourages the production of short 

 pectic chains. This model has many attractive features since, as con- 

 sideration will reveal, many aspects of cell wall softening can be in- 

 terpreted within this one framework. The particularly unattractive 

 feature of the model lies, however, in the fact that it would seem to 

 be most difficult to discover whether it corresponds to reality. 



LITERATURE CITED 



1. Albersheim, P., and Bonner, J. Metabolism and hormonal control of pectic 

 substances. Jour. Biol. Chem. 234: 3105-3108. 1959. 



2. Bennet-Clark, T. A., and KefEord, N. P. The extension growth-time relationship 

 for Avena coleoptile sections. Jour. Exper. Bot. 5: 293-304. 1954. 



3. Bishop, C. T., Bailey, S. T., and Setterfield, G. Chemical constitution of the 

 primary cell walls of Avena coleoptiles. Plant Physiol. 33: 283-289. 1958. 



4. Bonner, J. The action of the plant growth hormone. Jour. Gen. Physiol. 

 17: 63-76. 1933. 



5. . Zum Mechanismus der Zellstreckung auf Grund der Micellarlehre. 



Jahrb. Wiss. Bot. 82: 377-412. 1935. 



6. . The growth and respiration of the Avena coleoptile. Jour. Gen. 



Physiol. 20: 1-11. 1936. 



7. , and Foster, R. J. The growth-time relationships of the auxin-induced 



growth in Avena coleoptile sections. Jour. Exper. Bot. 6: 293-302. 1955. 



