Phytotropins such as 1-N-naphthylphthalamic acid (NPA) strongly inhibit auxin efflux, but the mechanism of this inhibition remains unknown. Auxin efflux is also strongly decreased by the vesicle trafficking inhibitor brefeldin A (BFA). Using suspension-cultured interphase cells of the BY-2 tobacco (Nicotiana tabacum L. cv Bright-Yellow 2) cell line, we compared the effects of NPA and BFA on auxin accumulation and on the arrangement of the cytoskeleton and endoplasmic reticulum (ER). The inhibition of auxin efflux (stimulation of net accumulation) by both NPA and BFA occurred rapidly with no measurable lag. NPA had no observable effect on the arrangement of microtubules, actin filaments, or ER. Thus, its inhibitory effect on auxin efflux was not mediated by perturbation of the cytoskeletal system and ER. BFA, however, caused substantial alterations to the arrangement of actin filaments and ER, including a characteristic accumulation of actin in the perinuclear cytoplasm. Even at saturating concentrations, NPA inhibited net auxin efflux far more effectively than did BFA. Therefore, a proportion of the NPA-sensitive auxin efflux carriers may be protected from the action of BFA. Maximum inhibition of auxin efflux occurred at concentrations of NPA substantially below those previously reported to be necessary to perturb vesicle trafficking. We found no evidence to support recent suggestions that the action of auxin transport inhibitors is mediated by a general inhibition of vesicle-mediated protein traffic to the plasma membrane.The polar transport of auxins (such as indole-3-acetic acid [IAA]) plays a crucial role in the regulation of growth and development in plants (Davies, 1995). Much experimental evidence supports the proposal by Rubery and Sheldrake (1974) and Raven (1975) that auxin transport polarity results from the differential permeabilities of each end of transporting cells to auxin anions (IAA Ϫ ) and undissociated auxin molecules (IAA; for review, see Goldsmith, 1977). IAA (a weak organic acid) is relatively lipophilic and can readily enter cells by diffusion from the more acidic extracellular space; the IAA Ϫ anion, on the other hand, is hydrophilic and does not cross membranes easily. As a consequence, auxins tend to accumulate in plant cells by a process of "anion trapping" and exit the symplast with the intervention of transmembrane auxin anion efflux carriers (Goldsmith, 1977). There is now overwhelming evidence that the differential efflux of IAA Ϫ anions from the two ends of auxin-transporting cells results from an asymmetric (polar) distribution of such carriers (Goldsmith, 1977;Lomax et al., 1995). Genes encoding putative auxin influx and efflux carriers have been identified from Arabidopsis and other species (for review, see Morris, 2000;Muday and DeLong, 2001;Friml and Palme, 2002). It has been shown that efflux carrier proteins, encoded by members of the PIN (PIN-FORMED) gene family, and possibly influx carriers (encoded by AUX1), are targeted to specific regions of the plasma membrane (PM) i...
Division and growth of most types of in vitro-cultured plant cells require an external source of auxin. In such cultures, the ratio of external to internal auxin concentration is crucial for the regulation of the phases of the standard growth cycle. In this report the internal concentration of auxin in suspension-cultured cells of Nicotiana tabacum L., strain VBI-0, was manipulated either (i) by increasing 10-fold the normal concentration of 1-naphthaleneacetic acid (NAA) and 2,4-dichlorophenoxyacetic acid in the external medium; or (ii) by addition 1-N-naphthylphthalamic acid (NPA; an inhibitor of auxin efflux and of auxin efflux carrier traffic). Both treatments delayed the onset of cell division for 6-7 days without loss of cell viability. In both cases, cell division activity subsequently resumed coincident with a reduction in the ability of cells to accumulate [(3)H]NAA from an external medium. Following renewed cell division, a significant proportion of the NPA-treated cells but not those grown at high auxin concentration, exhibited changes in the orientation of new cell divisions and loss of polarity. We conclude that cell division, but not cell elongation, is prevented when the internal auxin concentration rises above a critical threshold value and that the directed traffic of auxin efflux carriers to the plasma membrane may regulate the orientation of cell divisions.
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