The Mechanism of Auxin Action

Summary 1. The article deals mainly with the last decade, although earlier work is briefly surveyed. 2. In general an effect of auxins in increasing cell wall extensibility has been verified, although there is no consistent correlation of growth rate with either elastic or plastic extensibility. There is a general tendency to regard the older methods of measuring extensibilities as too drastic and therefore misleading. 3. Two phases in cell elongation have been recognized, namely, an initial phase of pure wall stretching and a subsequent phase of wall growth by intussusception. Auxins may stimulate the first phase by increasing the swelling capacity of the intermicellar colloids (pectins) through the intermediary of the living protoplasm. The phase of intussusception may also be affected. Most recent theories suggest that these actions are effected by a disturbance of the intramolecular forces concerned in the formation and maintenance of the molecular lattice of the young cell wall (Diehl et al., Burström). 4. The maintenance of cellular osmotic pressures during active elongation has suggested an active solute uptake mediated by an auxin‐augmented respiratory process as the cause of cell elongation (Commoner). The results do not justify these conclusions. 5. The early claims of J. Bonner of a stimulation of respiration by auxin in Avena coleoptiles have been verified under certain experimental conditions. It seems possible that the degree of this stimulation may be influenced by the presence of various components of the Gyorgyi C 4 dicarboxylic acid respiration cycle, which occurs in Avena coleoptiles. The use of monoiodoacetic acid as a differential inhibitor is misleading and results so far afford no proof of the action of auxins as a coenzyme in the C 4 ‐acid cycle. 6. Auxin has no effect on the in vitro activity of a wide range of dehydrogenases extracted from Avena coleoptiles or on catalase and some plant oxidases. The heightened dehydrogenase activity of auxin‐treated coleoptiles may be due to an in vivo activation (Berger & Avery) or to an active enzyme synthesis. 7. The production of simple sugars from carbohydrate reserves after auxin application is not due to an activation of diastase or to its ‘elution’ by auxin from a protective colloid. This shift in the starch → sugar equilibrium is probably secondary to the main action of auxin. 8. The original postulates of Koepfli, Thimann & Went concerning the minimum molecular requirements for auxin activity have been verified by all recent work. Most evidence supports the view that auxin is effective only in the undissociated state and not as an anion. It seems unlikely from polarographic investigations that auxins act as respiratory coenzymes by virtue of a reversible oxido‐reduction of the essential double bond in the ring. Physiological activity is probably associated with an essential high (lipophilic) surface activity of the ring and its double bond(s), the polar ‐COOH group being most effective when orientated perpendicular to the plane of this ring. 9. An auxin‐induced lowering of the protoplasmic structural viscosity has suggested a dissociating action on the complex plasma proteins (Northen). The resulting heightening of cell activity could originate the many diverse phenomena evoked by auxins. Such an effect on the ‘cytoskeleton’ is supported by the antagonistic action of certain quinonoid compounds (Jones). The acceleration of protoplasmic streaming by auxins and the interaction of malate still needs verification. More direct experiments are necessary to check the suggestion (Veldstra) that auxins regulate permeability, and therefore growth, after adsorption at a lipoid interface in the cell membrane. 10. Studies on the interaction of the auxins have thrown doubt on the ‘hemiauxin’ hypothesis of Went and suggest their action as coenzymes (Skoog). Further experimental data are required. Interactions with other cell metabolites are relatively unexplored, but offer profitable lines for research. 11. The general conclusion drawn is that most recent theories tend to be too restricted and superficial, and, unless auxin exerts a number of discrete effects in different cell systems, we must look deeper for a more fundamental action (e.g. the theories of Northen) to explain the whole range of relevant phenomena.