On Auxin Antagonists and Synergists in Root Growth

ÅBerg, Börje

doi:10.1111/j.1399-3054.1950.tb07673.x

Cited by 63 publications

(11 citation statements)

References 31 publications

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“…The 2, 5-derivative seemed to be the most active. In our hands the 2,6-isomer gave the greatest growth response, while 2, 3-and 2, The failture of TIBA to promote pith growth confirms the data of Niedergang-Kamien and Skoog (25) for stem segments containing vascular tissue, but is at variance with its reported synergistic effect on low levels of endogenous auxin (31) or added IAA (1,31), and its reported stimtulation of section growth (21). These differences can be accounted for on the basis of the strong inhibition by TIBA of polar auxin transport.…”

Section: Discussionsupporting

confidence: 88%

Auxin Activity of Substituted Benzoic Acids and Their Effect on Polar Auxin Transport

Keitt

Baker

1966

Plant Physiol.

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Summinary. Six dichloro-, 3 trichloro-, 2 triiodo-, and 3 heterosubstituted benzoic acids (amiben, dinoben, dicamba), and N-1-naphthylphthalamic acid have been tested for effects on growth and on polar auxin transport. Growth activity with and without kinetin was measured by effects on fresh and dry weights of 30-day cultures of fresh tobacco pith. Transport inhibition was measured by following uptake and output of IAA-2-14C through 10 mm bean epicotyl sections. The distribution of callus growth on vascularized tobacco stem segments was also observed. Avena first internode extension assays established the relative activities: dicamba> amiben> dinoben suggested by pith growth results. Growth effects of active compounds were similar with and without kinetin, except that amiben was less active with kinetin, while 2, 3, 6-trichlorobenzoic acid was more active with kinctin than alone. The weak auxin activity of NPA was confirmed. Transport experiments showed that NPA was the most inhibitory compound tested, followed by TIBA. Other compounds tested were at least 300 times less inhibitory to IAA transport. The best growth promoters were the least inhibitory to transport, and the most effective transport inhibitors were at best poor auxins. It is suggested that the weak auxin and auxin synergistic activity of TIBA (and perhaps 2, 3-dichlorobenzoic acid) in extension growth tests arises from its inhibition of transport of endogenous or added auxin out of the sections, rather than from its intrinsic auxin activity. Chemically induced apolar callus growth on vascularized tobacco stem explants can arise from inhibition of native auxin transport, apolar growth stimulation by auxinic action of the test compound, or both.Prior studies (10,11,20,22,23,24,25,32) of the effect of chemicals on polar auxin transport have shown that those which A) interfere with ATP formation ( 3DNP), B) are sulfhydryl binders (TIBA, iodoacetate, PCMB) or C) are weak (NPA, 2,5-dichlorobenzoic acid) or strong (2,4-D) auxins can all decrease the amount of IAA reaching a receptor block from the basal end of a section of stem tissue to whose apical end it has been applied. A limited survey of 10 phenoxyacetic acids (24) showed that transport inhibition increased with the number of substituted chlorine atoms up to 3, and that the active molecules tended to have higher This studN' was aided by funds from the National Science Foundation, Grants C 14545 and GB 153.2 Present address: Department of Botany, Duke University, Durham, North Carolina. 3 The following abbreviations and trivial names are used throughout: DNP = 2,4-dinitrophenol, NPA = N-1-naphthylphthalamic acid, PCMB = p-chlorophenylmercuribenzoate, 'rIBA -2,3,5-triiodobenzoic acid, amiben = 3-amino-2,4-dichlorobenzoic acid, dicamba = 2,5-dichloro-6-methoxv benzoic acid, dinobein = 2,5-dichloro-3-nitrobenzoic acid.

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Section: Discussionsupporting

confidence: 88%

Auxin Activity of Substituted Benzoic Acids and Their Effect on Polar Auxin Transport

Keitt

Baker

1966

Plant Physiol.

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“…To this end, we screened seedlings on p ‐chlorophenoxyisobutyric acid (PCIB), a chemical thought to inhibit early auxin signaling events. Although PCIB is structurally similar to some synthetic auxins (Jönsson, 1961), many years ago it was shown to inhibit several auxin‐induced physiological responses competitively (Åberg, 1950, 1951; Burström, 1950). Consistent with these results, Oono et al.…”

Section: Introductionmentioning

confidence: 99%

A small acidic protein 1 (SMAP1) mediates responses of the Arabidopsis root to the synthetic auxin 2,4‐dichlorophenoxyacetic acid

et al. 2006

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Summary 2,4-dichlorophenoxyacetic acid (2,4-D), a chemical analogue of indole-3-acetic acid (IAA), is widely used as a growth regulator and exogenous source of auxin. Because 2,4-D evokes physiological and molecular responses similar to those evoked by IAA, it is believed that they share a common response pathway. Here, we show that a mutant, antiauxin resistant1 (aar1), identified in a screen for resistance to the anti-auxin p-chlorophenoxyisobutyric acid (PCIB), is resistant to 2,4-D, yet nevertheless responds like the wild-type to IAA and 1-napthaleneacetic acid in root elongation and lateral root induction assays. That the aar1 mutation alters 2,4-D responsiveness specifically was confirmed by analysis of GUS expression in the DR5:GUS and HS:AXR3NT-GUS backgrounds, as well as by real-time PCR quantification of IAA11 expression. The two characterized aar1 alleles both harbor multi-gene deletions; however, 2,4-D responsiveness was restored by transformation with one of the genes missing in both alleles, and the 2,4-D-resistant phenotype was reproduced by decreasing the expression of the same gene in the wild-type using an RNAi construct. The gene encodes a small, acidic protein (SMAP1) with unknown function and present in plants, animals and invertebrates but not in fungi or prokaryotes. Taken together, these results suggest that SMAP1 is a regulatory component that mediates responses to 2,4-D, and that responses to 2,4-D and IAA are partially distinct.

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“…This supposition would imply not only that auxins become attached in the plant but also that diverse auxins exert their effects through attachment at a common site. That these suppositions are correct has been strongly indicated by the fact that any given antiauxin inhibits the effects of many, perhaps of all, different auxins (1,9,14).…”

Section: Introductionmentioning

confidence: 99%