title: Ion fluxes, auxin and the induction of elongation growth in Nicotiana tabacum cells.
abstract: Immobilized cultured tobacco cells become polarized upon the addition of naphthalene-1-acetic acid and start to elongate from an initial spherical shape. The question as to how a diffuse-growing cell forms a polar axis is addressed here with approaches successfully applied to the study of tip growth. With two kinds of vibrating probes the electric current flow and proton fluxes were mapped around such elongating cells. No consistent polar pattern of ion fluxes, which is typical for actively tip-growing cells, was detected. Therefore, other signals must provide the positional information needed for polar axis formation. Furthermore, neither a specific pattern of intracellular Ca(2+) concentration nor a polar distribution of putative ion-channel antagonist-binding sites were found in elongating tobacco cells. Auxin flux, on the other hand, was found to be important as TIBA, an inhibitor of polar auxin transport, clearly inhibited elongation in a concentration-dependent way. Cross-linking of arabinogalactan-proteins with the beta-Yariv reagent also resulted in inhibition of elongation. A model is proposed for the induction of polar growth where localized auxin efflux starts a signal cascade that triggers molecules that reorient microtubules. These then guide cellulose deposition in the cell wall, which in turn alters cell wall mechanics and leads to elongation. In this scheme, arabinogalactan-proteins are not causal agents but are probably important regulators of growth and survival of the cell.
authors.affiliation: Department of Biology, Plant Physiology/Morphology, University of Antwerp (UIA), Universiteitsplein 1, B-2610 Wilrijk, Belgium.
authors.forename: K
authors.initials: K
authors.lastname: Vissenberg
authors.forename: J A
authors.initials: JA
authors.lastname: Feijó
authors.forename: M H
authors.initials: MH
authors.lastname: Weisenseel
authors.forename: J P
authors.initials: JP
authors.lastname: Verbelen
mesh_terms: D001665:Binding Sites; D001667:Binding, Competitive; D001692:Biological Transport / Q000187:drug effects; D002121:Calcium Channel Blockers / Q000378:metabolism; D015220:Calcium Channels / Q000378:metabolism; D002455:Cell Division / Q000187:drug effects / Q000502:physiology; D002478:Cells, Cultured; D003599:Cytoskeleton / Q000187:drug effects / Q000502:physiology; D004305:Dose-Response Relationship, Drug; D005960:Glucosides / Q000494:pharmacology; D007210:Indoleacetic Acids / Q000502:physiology*; D017136:Ion Transport / Q000502:physiology*; D008954:Models, Biological; D009280:Naphthaleneacetic Acids / Q000494:pharmacology; D010696:Phloroglucinol / Q000031:analogs & derivatives* / Q000494:pharmacology; D018547:Plant Stems / Q000187:drug effects / Q000502:physiology; D011523:Protoplasts / Q000187:drug effects / Q000502:physiology; D015398:Signal Transduction / Q000187:drug effects / Q000502:physiology; D014026:Nicotiana / Q000166:cytology / Q000187:drug effects / Q000378:metabolism*; D014283:Triiodobenzoic Acids / Q000494:pharmacology
chemical_list: D002121:Calcium Channel Blockers; D015220:Calcium Channels; D005960:Glucosides; D007210:Indoleacetic Acids; D009280:Naphthaleneacetic Acids; D014283:Triiodobenzoic Acids; C104977:Yariv reagent; C034182:1-naphthaleneacetic acid; D010696:Phloroglucinol; C052968:2,3,5-triiodobenzoic acid