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Robert E. Cleland Graham Buckley Sogol Nowbar Nina M. Lew Charles Stinemetz Michael L. Evans David L. Rayle 《Planta》1991,186(1):70-74
The acid-growth theory predicts that a solution with a pH identical to that of the apoplast of auxintreated tissues (4.5–5.0) should induce elongation at a rate comparable to that of auxin. Different pH profiles for elongation have been obtained, however, depending on the type of pretreatment between harvest of the sections and the start of the pH-incubations. To determine the acid sensitivity under in vivo conditions, oat (Avena sativa L.) coleoptile, maize (Zea mays L.) coleoptile and pea (Pisum sativum L.) epicotyl sections were abraded so that exogenous buffers could penetrate the free space, and placed in buffered solutions of pH 3.5–6.5 without any preincubation. The extension, without auxin, was measured over the first 3 h. Experiments conducted in three laboratories produced similar results. For all three species, sections placed in buffer without pretreatment elongated at least threefold faster at pH 5.0 than at 6.0 or 6.5, and the rate elongation at pH 5.0 was comparable to that induced by auxin. Pretreatment of abraded sections with pH-6.5 buffer or distilled water adjusted to pH 6.5 or above gave similar results. We conclude that the pH present in the apoplast of auxin-treated coleoptile and stems is sufficiently low to account for the initial growth response to auxin.Abbreviations FS
free space
- IAA
indole-3-acetic acid
This research was supported by a grant from the National Adonautics and space Administration (NASA), NAGW 1394 to R.E.C., NASA grant NAGW-297 to M.L.E., and NASA grant NAG 1849 to D.L.R. 相似文献
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The rheological properties of corn (Zea mays L. cv. Garant) root elongation zones were investigated by means of a computer-controlled extensiometer. Creep closely followed
a logarithmic time function, which was used to quantify creep activity. Pretreatment with auxin, which inhibits extension
growth in roots, lowered the creep activity and the apparent plastic extensibility. While the time course of the inhibition
of apparent plastic extensibility lagged behind the cessation of elongation growth, the drop in creep activity matched the
growth inhibition more closely. Creep activity and apparent plastic extensibility were not significantly affected by pH. These
data support the view that the auxin-induced cell wall stiffening (e.g. by cross-linking processes), while causal for the
growth inhibition, is not brought about by a cell wall alkalinization.
Received: 10 December 1996 / Accepted: 19 August 1997 相似文献
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Elongation growth of plant cells occurs by stretching of cell walls under turgor pressure when intermolecular bonds in the
walls are temporarily loosened. The acid-growth theory predicts that wall loosening is the result of wall acidification because
treatments (including IAA and fusicoccin) that cause lowered wall pH cause elongation. However, conclusive evidence that IAA
primarily reduces wall pH has been lacking. Calcium has been reported to stiffen the cell walls. We have used a microelectrode
ion-flux measuring technique to observe directly, and non-invasively, the net fluxes of protons and calcium from split coleoptiles
of oats (Avena sativa L.) in unbuffered solution. Normal net fluxes are 10 nmol · m−2 · s−1 proton efflux and zero calcium flux. The toxin fusicoccin (1 μM) causes immediate efflux from tissue not only of protons,
but also of calcium, about 110 nmol · m−2 · s−1 in each case. The data fit the “weak acid Donnan Manning” model for ion exchange in the cell wall. Thus we associate the
known “acid-growth” effect of fusicoccin with the displacement of calcium from the wall by exchange for protons extruded from
the cytoplasm. Application of 10 μM IAA causes proton efflux to increase transiently by about 15 nmol · m−2 · s−1 with a lag of about 10 min. The calcium influx decreases immediately to an efflux of about 20 nmol · m−2 · s−1. It appears that auxin too causes an “acid-growth” effect, with extruded protons exchanging for calcium in the cell walls.
I. Arif is currently recieving an AIDAB scholarship. This work was supported by an Australian Research Council grant to I.A.
Newman. 相似文献
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Light-induced expansion of Phaseolus vulgaris L. leaf cells is accompanied by increased cell-wall plasticity. The possibility that leaf-cell walls are loosened by excreted protons has been investigated. First, light causes acidification, detected at the leaf surface, within 5–15 min. Growth starts 10–20 min after exposure to light. Second, exogenous acid induces loosening of isolated leaf cell walls. Third, infiltration of the tissue with a neutral buffer inhibits light-induced growth. Fourth, fusicoccin stimulates growth of as well as H+ excretion by bean leaf cells, without light. These findings show that the acid-growth theory is applicable to light-induced growth of leaf cells, and indicate that light-induced proton excretion initiates cell enlargement in leaves.Abbreviations FC
fusicoccin
- RL
red light
- WEx
wall extensibility
- WL
white light 相似文献
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Four experimental predictions of the acid-growth theory of auxin (indole-3-acetic acid, IAA) action in inducing cell elongation were reinvestigated using abraded segments of maize (Zea mays L.) coleoptiles. i) Quantitative comparison of segment elongation and medium-acidification kinetics measured in the same sample of tissue reveals that these IAA-induced processes are neither correlated in time nor responding coordinately to cations present in the medium. ii) Exogenous protons are not able to substitute for IAA in causing segment elongation at the predicted pH of 4.5–5.0. Instead, external buffers induce significant segment elongation only below pH 4.5, reaching a maximal response at pH 1.75–2.5. Acid and IAA coact additively, and therefore independently, in the whole range of feasible pH values. iii) Neutral or alkaline buffers (pH 6–10) are unable to abolish the IAA-mediated growth response and have no effect on its lag-phase. iv) Fusicoccin, at a concentration producing the same H+ excretion as high concentrations of IAA, is ineffective in inducing segment elongation. Moreover, sucrose and other sugars can quantiatively substritute for IAA in inducing H+ excretion but are likewise ineffective in inducing elongation. It is concluded that these results are incompatible with the acid-growth theory of auxin action.Abbreviations IAA
indole-3-acetic acid
- FC
fusicoccin 相似文献
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Three predictions of the acid-growth theory of fusicoccin (FC) action in inducing cell elongation were reinvestigated using abraded segments of maize (Zea mays L.) coleoptiles. i) Quantitative comparison of segment elongation and medium-acidification kinetics measured in the same sample of tissue shows that these FC-induced processes are strictly correlated in time and respond coordinately to cations present in the medium. ii) Fusicoccin (1 mol l-1) induces a rapid acidification of the cell-wall solution, reaching a final level of pH 3.8–4.0. Exogenous protons are able to substitute quantitatively for FC in causing segment elongation at pH 3.8–4.0. At pH 4, FC has no additional effect on cell elongation. iii) Neutral buffers (pH 7) completely abolish the FC-mediated growth response. iv) Cycloheximide (10 mg l-1) inhibits both FC-induced and acid-buffer(pH 4)-induced elongation after a lag of 40–45 min, and FC-induced H+ excretion after a lag of 2 h. Under the same conditions, indole-3-acetic acid-induced elongation and H+ excretion are inhibited without detectable lag. It is concluded that these results are fully compatible with the acid-growth theory of FC action.Abbreviations IAA
indole-3-acetic acid
- CHI
cycloheximide
- FC
fusicoccin 相似文献
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The elongation growth of etiolated hypocotyl segments of lupin (Lupinus albus L.) was stimulated by acid pH (4.6 versus 6.5) and by IAA for periods of up to 4 h. After this time, the segments were unable to grow further. In the presence of an optimal IAA concentration (10 μM), acid pH increased the growth rate but had no effect on final growth. With suboptimal IAA (0.1 μM), however, acid pH increased growth in a more than additive way, suggesting a synergistic action between the two factors. This synergism may be explained by the increased IAA uptake and decarboxylation seen at an acid pH. These results reinforce the view that the effects of low pH and IAA on growth are not independent. Vanadate inhibited growth and also IAA uptake and decarboxylation. This inhibitor, therefore, probably inhibits growth not only by decreasing ATPase-mediated acidification but also by decreasing H+-dependent IAA uptake from the apoplasm. This dependence of IAA uptake on ATPase may be mediated by apoplasmic acidification. The amount of IAA decarboxylated increased when the assay conditions favored the growth of segments, indicating that IAA could be destroyed by decarboxylation during the auxin-induced growth. 相似文献
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Role of the plasma membrane H<Superscript>+</Superscript>-ATPase in auxin-induced elongation growth: historical and new aspects 总被引:3,自引:0,他引:3
Hager A 《Journal of plant research》2003,116(6):483-505
This article will cover historical and recent aspects of reactions and mechanisms involved in the auxin-induced signalling cascade that terminates in the dramatic elongation growth of cells and plant organs. Massive evidence has accumulated that the final target of auxin action is the plasma membrane H+-ATPase, which excretes H+ ions into the cell wall compartment and, in an antiport, takes up K+ ions through an inwardly rectifying K+ channel. The auxin-enhanced H+ pumping lowers the cell wall pH, activates pH-sensitive enzymes and proteins within the wall, and initiates cell-wall loosening and extension growth. These processes, induced by auxin or by the "super-auxin" fusicoccin, can be blocked instantly and specifically by a voltage inhibition of the H+-ATPase due to removal of K+ ions or the addition of K+-channel blockers. Vice versa, H+ pumping and growth are immediately switched on by addition of K+ ions. Furthermore, the treatment of segments either with auxin or with fusicoccin (which activates the H+-ATPase irreversibly) or with acid buffers (from outside) causes an identical transformation and degradation pattern of cell wall constituents during cell-wall loosening and growth. These and other results described below are in agreement with the acid-growth theory of elongation growth. However, objections to this theory are also discussed. 相似文献
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