Auxin-Regulated Cell Enlargement: Is there Action at the Level of Gene Expression?

Vanderhoef, Larry N.

doi:10.1007/978-1-4613-3051-6_13

Cited by 19 publications

(17 citation statements)

References 22 publications

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“…The unusual early elongation kinetics led first to the postulate that there were separable responses (20), then to the conclusion that elongation during the early phase of elongation (in auxinstimulated elongation in excised segments) was biochemically distinct from elongation during the later phase (8,21,23), and fmally to an explanation of the two phases (this manuscript and refs. 15 …”

Section: Discussionmentioning

confidence: 99%

“…We suggested, and others have confirmed (8), that auxin-induced elongation could be separated into two phases, the early burst of growth (simulated by lowering the pH from 6 to 4) and a later phase associated with long-term, steady-state growth. Subsequent experiments showed that elongation during the first phase was biochemically distinct from elongation during the second phase (15,16,21,23 This suggested sequence of events in the excised segment allows a testable prediction: if the wail is kept loose from the moment of excision and throughout the preincubation (during auxin depletion), then reinitiation of elongation by exogenous auxin should occur in the absence of the short-lag burst of growth which occurs during wall loosening. That is, exogenous auxin should induce just the second response.…”

Section: Methodsmentioning

confidence: 99%

“…We suggested, and others have confirmed (8), that auxin-induced elongation could be separated into two phases, the early burst of growth (simulated by lowering the pH from 6 to 4) and a later phase associated with long-term, steady-state growth. Subsequent experiments showed that elongation during the first phase was biochemically distinct from elongation during the second phase (15,16,21,23 Figure 1. The figure is based on the data that prove the existence of separable responses, on the data which support the wall-acidification and gene expression hypotheses and on the consideration of what very likely happens to an excised rapidly elongating segment which is preincubated and then treated with acid or auxin.…”

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Auxin-regulated Wall Loosening and Sustained Growth in Elongation

Vanderhoef

Dute²

1981

Plant Physiol.

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It is proposed that auxin regulates and coordinates both wail loosening and the supply of wall materials in elongation. The Experiments reported herein support the proposal that auxin coordinates wall loosening and the supply of wall materials in its regulation of cell elongation. MATERIALS AND METHODSSoybean seedlings (Glycine max L. Merr. var. Wayne) were germinated in the dark for 3 days, and the elongating segment of the hypocotyl was excised as described (20,22). Pea seedlings, Pisum sativum var. Alaska, were germinated in the dark in moist vermiculite at 25 C for 4 days. Elongating segments were excised from the first internode of the epicotyl immediately below the hook. Hypocotyl and epicotyl extension were measured continuously with a linear position-sensitive transducer in an apparatus modified after that reported (19), except that the clamped segments were immersed in 25 C medium. The pH 6 medium, 5 mM Kphosphate, and the pH 4 medium, 5 iim K-citrate, contained 30 mm sucrose. IAA was added to a final concentration of 45 ,uM in the soybean experiments.The mode of action of auxin-regulated elongation is not known. Recently, two hypotheses have guided research in this area. In the 1960s, the gene expression hypothesis proposed that auxin regulated wall loosening and steady-state elongation by action at gene transcription or translation (9,14). However, recognition of the short lag between auxin application and detectable elongation rate increase (10,12,25) by Evans and Ray (6) was thought to rule out primarily mediation at gene expression in auxin-regulated wall loosening (11). In 1971, the wall-acidification hypothesis (4, 13) was independently proposed by Hager et al. (7) and Cleland (3). This hypothesis, which proposes that auxin regulates wall loosening by causing a pH drop in the area of the cell wall, has survived a series of rigorous challenges (4). The molecular mechanism of auxin-caused wall acidification remains to be described.In 1975, we commented on the unusual early kinetics which are seen when auxin stimulates elongation in auxin-depleted (hence, slowly growing), excised elongating segments (20). We suggested, and others have confirmed (8), that auxin-induced elongation could be separated into two phases, the early burst of growth (simulated by lowering the pH from 6 to 4) and a later phase associated with long-term, steady-state growth. Subsequent experiments showed that elongation during the first phase was biochemically distinct from elongation during the second phase (15,16,21,23 Figure 1. The figure is based on the data that prove the existence of separable responses, on the data which support the wall-acidification and gene expression hypotheses and on the consideration of what very likely happens to an excised rapidly elongating segment which is preincubated and then treated with acid or auxin. The figure depicts two auxin activities in the control of growth, wail loosening and the regulation of the supply of wall materials. During steady-state growth in the intact plant, t...

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Section: Discussionmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

“…We suggested, and others have confirmed (8), that auxin-induced elongation could be separated into two phases, the early burst of growth (simulated by lowering the pH from 6 to 4) and a later phase associated with long-term, steady-state growth. Subsequent experiments showed that elongation during the first phase was biochemically distinct from elongation during the second phase (15,16,21,23 Figure 1. The figure is based on the data that prove the existence of separable responses, on the data which support the wall-acidification and gene expression hypotheses and on the consideration of what very likely happens to an excised rapidly elongating segment which is preincubated and then treated with acid or auxin.…”

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Auxin-regulated Wall Loosening and Sustained Growth in Elongation

Vanderhoef

Dute²

1981

Plant Physiol.

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“…One system that has proven to be a useful model for studying the molecular mechanisms underlying hormonally induced changes in gene expression has been auxin-induced cell elongation (e.g. 12,18,23,26). As part of our laboratory's studies of hormonal control of gene expression, we have isolated cDNA clones, pJCWI and pJCW2, for two auxin-responsive mRNAs from the elongating region of the soybean hypocotyl (24).…”

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confidence: 99%

An Analysis of Growth Regulator Interactions and Gene Expression during Auxin-Induced Cell Elongation Using Cloned Complementary DNAs to Auxin-Responsive Messenger RNAs

Walker

Legocka²,

Edelman³

et al. 1985

Plant Physiol.

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We have examined the effects of cytokinin, fusicoccin, and ethylene on auxin-induced changes in gene expression during auxin-promoted cell elongation in soybean (Glycine max L. Meff. cv Wayne) using cloned cDNAs to two auxin-responsive mRNAs (Walker, Key 1982 Proc Natl Acad Sci USA 79: . RNA blot analyses demonstrate that under conditions of cytokinin inhibition of auxin-promoted cell elongation the levels of these two auxin-responsive mRNAs is unaltered. Fusicoccinpromoted elonption is not associated with an enhanced expression of these two mRNAs, suggesting that the increased levels of these mRNAs observed during auxin-promoted cell elongation are not simply due to enhanced rates of cell elonption. We have also determined that ethylene plays no apparent role in the regulation of expression of these mRNAs. However, the auxins indole-3-acetic acid, 2,4-dichlorophenoxyacetic acid, and a-naphthalene acetic acid all enhance an accumulation of these mRNAs. We conclude that the regulation of these mRNAs is directly dependent on auxin. That auxin-promoted cell elongation is dependent upon the increased accumulation of these mRNAs remains to be determined.In recent years a considerable amount of evidence has accumulated indicating that all classes of plant hormones can cause selective changes in the levels of specific mRNAs (e.g. 3, 6, 8, 21). One system that has proven to be a useful model for studying the molecular mechanisms underlying hormonally induced changes in gene expression has been auxin-induced cell elongation (e.g. 12, 18, 23, 26 23, 25, and 50 uM, respectively (see 11 and references cited therein); FC was used at 10 JuM (see 14 and references cited therein); IPA was used at 50 uM (22). In experiments using ethylene, ethylene in air (10 ul/1) was gently bubbled into the incubation medium and allowed to exit through a second hole in the stoppered flask into 50% (v/v) ethanol. AVG was used at 100 ,M and ACC at 1 mM (9); all incubations using these compounds were performed in stoppered flasks. IAA, 2,4-D, a-NAA, IPA, AOA, and ACC were obtained from Sigma; AVG was a gift of W

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“…However, the contribution that this induced gene expression makes to the mechanism of auxin regulated cell wall elongation has not yet been determined. The observation that there are two separate elongation responses to auxin in higher plants, one which may ready the wall for the process of elongation and a second which requires the action of newly synthesized gene products, has led to the suggestion that the distinctly different models of gene expression and wall acidification initially proposed are not incompatible (15).…”

Section: Abstracirmentioning

confidence: 99%