THE EFFECTS OF SYNTHETIC GROWTH 



SUBSTANCES IN THE LEVEL OF 



ENDOGENOUS AUXINS IN PLANTS! 



L. J. AuDUS and Ruth Thresh 

 Bedford College, University of London 



Currently fashionable theories of auxin and anti-auxin activity hinge on the 

 assumption of direct actions of the active molecules at growth centres. The 

 interactions of these substances in their effects on growth are thereby 

 explained by competition for these specific sites of action. We wish, however, 

 in this paper to revert to older, somewhat less fashionable, theories which 

 suppose that synthetic organic molecules, having an effect on the growth of 

 plant organs, may not be acting in this direct manner but that their activities 

 may be due to a disturbance of the level of natural endogenous auxins. 

 We recall the theory advanced by Skoog in 1947. It was then suggested that 

 the activity of 2:4-dichlorophenoxyacedc acid (2:4-D) might be attributed 

 to its competitive release of bound natural auxin from protein surfaces, 

 where it was held inactive, so that it became free and available to affect 

 growth. Theories involving a disturbance of native auxin metabolism have 

 been put forward to account for the activity of certain supposed anti-auxins 

 (e.g. maleic hydrazide; Aberg, 1953). In spite of considerable evidence to 

 the contrary, it seemed to us some three years ago that these theories were 

 still well worth considering and worth the effort of experimental testing. 

 The obvious attack on the problem was to treat susceptible plants with 

 synthetic growth 'regulators' at levels producing characteristic growth 

 responses but well below toxicity limits. Subsequent paper partidon 

 chromatography of extracts and quantitative assay of the active compounds 

 thus separated should reveal any disturbance of endogenous auxin levels and 

 throw direct light on the validity of these early theories. During the progress 

 of the work there have appeared papers dealing with the effects of 2:4-D 

 (Weintraub, 1953; Henderson and Deese, 1954) and maleic hydrazide 

 (Kulescha, 1953; Pilet, 1953) on endogenous auxin levels in various tissues. 

 The accuracy of these assays, however, may have been completely vitiated 

 by residual 2:4-D or maleic hydrazide (MH) in the extracts and so they 

 need not be further considered. Chromatographic assays should be free 

 from these objections, 



EXPERIMENTAL 



Three synthetic compounds were chosen for study, 2:4-D, on account of its 

 very high 'auxin' activity, maleic hydrazide, because of its suspected action 

 as a metabolic antagonist of auxin, and 2:3:5-triiodobenzoic acid (TIBA), 

 because of its structural similarity to the growth-promoting subsdtuted 

 benzoic acids and the plausibility of its competitive acdon at a growth centre 

 or at some other auxin-binding site in the cell. 

 f This paper was read at the Conference by L. J. Audus. 



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