Transport and metabolism of xylem cytokinins during lateral bud release in decapitated chickpea (<i>Cicer arietinum</i>) seedlings

Mader, Johanna C.; Turnbull, Colin; Emery, R. J. Neil

doi:10.1034/j.1399-3054.2003.1170115.x

Cited by 20 publications

(17 citation statements)

References 44 publications

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“…This includes all nodes analyzed above girdle sites and also in the node harvested below the girdle situated between nodes 3 and 4. This strong correlation between bud outgrowth and IPT1 and IPT2 expression, and thus presumably CK biosynthesis (Miyawaki et al, 2004;Nordstrom et al, 2004;Tanaka et al, 2006), supports previous suggestions of an important requirement of CK in bud outgrowth (Pillay and Railton, 1983;Medford et al, 1989;Bangerth, 1994;Cline et al, 1997Cline et al, , 2006Li and Bangerth, 2003;Mader et al, 2003aMader et al, , 2003bNakagawa et al, 2005).…”

Section: Cytokinin Biosynthetic Gene Expression Correlates With Bud Osupporting

confidence: 89%

Roles for Auxin, Cytokinin, and Strigolactone in Regulating Shoot Branching

2009

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Many processes have been described in the control of shoot branching. Apical dominance is defined as the control exerted by the shoot tip on the outgrowth of axillary buds, whereas correlative inhibition includes the suppression of growth by other growing buds or shoots. The level, signaling, and/or flow of the plant hormone auxin in stems and buds is thought to be involved in these processes. In addition, RAMOSUS (RMS) branching genes in pea (Pisum sativum) control the synthesis and perception of a long-distance inhibitory branching signal produced in the stem and roots, a strigolactone or product. Auxin treatment affects the expression of RMS genes, but it is unclear whether the RMS network can regulate branching independently of auxin. Here, we explore whether apical dominance and correlative inhibition show independent or additive effects in rms mutant plants. Bud outgrowth and branch lengths are enhanced in decapitated and stem-girdled rms mutants compared with intact control plants. This may relate to an RMS-independent induction of axillary bud outgrowth by these treatments. Correlative inhibition was also apparent in rms mutant plants, again indicating an RMS-independent component. Treatments giving reductions in RMS1 and RMS5 gene expression, auxin transport, and auxin level in the main stem were not always sufficient to promote bud outgrowth. We suggest that this may relate to a failure to induce the expression of cytokinin biosynthesis genes, which always correlated with bud outgrowth in our treatments. We present a new model that accounts for apical dominance, correlative inhibition, RMS gene action, and auxin and cytokinin and their interactions in controlling the progression of buds through different control points from dormancy to sustained growth.

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Section: Cytokinin Biosynthetic Gene Expression Correlates With Bud Osupporting

confidence: 89%

Roles for Auxin, Cytokinin, and Strigolactone in Regulating Shoot Branching

2009

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“…In SL-deficient rms mutants, alternative auxin targets such as suppression of local CK biosynthesis may provide the explanation for bud inhibition in isolated rms nodes. By contrast, additional CK arriving from roots of decapitated plants (Foo et al, 2007) is significantly redirected to bud tissues by decapitation (Mader et al, 2003) and may not be inhibited by auxin. Supporting evidence comes from the differences in CK profiles: Auxin suppressed tZ-type CKs in decapitated stems much less than in corresponding explants, whereas levels of other CKs were comparable between the two treatments.…”

Section: Conditional Auxin Response In Rms Mutants May Be Due To Addimentioning

confidence: 90%

Conditional Auxin Response and Differential Cytokinin Profiles in Shoot Branching Mutants

et al. 2014

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Strigolactone (SL), auxin, and cytokinin (CK) are hormones that interact to regulate shoot branching. For example, several ramosus (rms) branching mutants in pea (Pisum sativum) have SL defects, perturbed xylem CK levels, and diminished responses to auxin in shoot decapitation assays. In contrast with the last of these characteristics, we discovered that buds on isolated nodes (explants) of rms plants instead respond normally to auxin. We hypothesized that the presence or absence of attached roots would result in transcriptional and hormonal differences in buds and subtending stem tissues, and might underlie the differential auxin response. However, decapitated plants and explants both showed similar up-regulation of CK biosynthesis genes, increased CK levels, and down-regulation of auxin transport genes. Moreover, auxin application counteracted these trends, regardless of the effectiveness of auxin at inhibiting bud growth. Multivariate analysis revealed that stem transcript and CK changes were largely associated with decapitation and/or root removal and auxin response, whereas bud transcript profiles related more to SL defects. CK clustering profiles were indicative of additional zeatin-type CKs in decapitated stems being supplied by roots and thus promoting bud growth in SL-deficient genotypes even in the presence of added auxin. This difference in CK content may explain why rms buds on explants respond better to auxin than those on decapitated plants. We further conclude that rapid changes in CK status in stems are auxin dependent but largely SL independent, suggesting a model in which auxin and CK are dominant regulators of decapitation-induced branching, whereas SLs are more important in intact plants.

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“…1C). Secondly, as cytokinins are transported in the xylem sap and the supply of solutes delivered in the xylem sap to axillary buds increases rapidly after decapitation, cytokinins or other xylem mobile molecules may play a role in the initial stage of bud release (Mader et al, 2003). Another possibility is that decapitation removes a sink for photosynthates and nutrients and that the increased availability of these substances initiates axillary bud outgrowth.…”

Section: Discussionmentioning

confidence: 99%

Auxin Dynamics after Decapitation Are Not Correlated with the Initial Growth of Axillary Buds

Morris

Cox²,

Ross³

et al. 2005

Plant Physiology

119

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One of the first and most enduring roles identified for the plant hormone auxin is the mediation of apical dominance. Many reports have claimed that reduced stem indole-3-acetic acid (IAA) levels and/or reduced basipetal IAA transport directly or indirectly initiate bud growth in decapitated plants. We have tested whether auxin inhibits the initial stage of bud release, or subsequent stages, in garden pea (Pisum sativum) by providing a rigorous examination of the dynamics of auxin level, auxin transport, and axillary bud growth. We demonstrate that after decapitation, initial bud growth occurs prior to changes in IAA level or transport in surrounding stem tissue and is not prevented by an acropetal supply of exogenous auxin. We also show that auxin transport inhibitors cause a similar auxin depletion as decapitation, but do not stimulate bud growth within our experimental time-frame. These results indicate that decapitation may trigger initial bud growth via an auxin-independent mechanism. We propose that auxin operates after this initial stage, mediating apical dominance via autoregulation of buds that are already in transition toward sustained growth.Decapitated garden pea (Pisum sativum) seedlings, bearing axillary buds in leaf axils separated by long internodes, were one of the first systems used to study apical dominance in plants (Snow, 1931). In pea, several axillary buds respond to decapitation by enlarging, but only a few of these reach sustained growth; dormancy remains imposed or is reimposed in the remainder (Stafstrom and Sussex, 1988). This autoregulation of shoot branching is achieved by longdistance signaling (for review, see Napoli et al., 1999). The transition of axillary buds from dormancy to sustained growth in vegetative shoots involves several developmental stages typified by expression of particular molecular markers (Stafstrom and Sussex, 1988;Napoli et al., 1999;Shimizu-Sato and Mori, 2001). The action of long-distance signals at any one or more of these stages could mediate apical dominance.It is well known that the application of auxin to the stump of decapitated plants inhibits axillary bud outgrowth, although less is known about the stage at which auxin acts. A frequently overlooked feature of this inhibition is that it is rarely complete with axillary buds usually growing a small but measurable amount prior to or during inhibition. The results of experiments with auxin transport inhibitors also appear to be consistent with a key role for auxin in apical dominance. These compounds are reported to promote lateral outgrowth (naphthylphtalamic acid [NPA], Tamas, 1987; 2,3,5-triiodobenzoic acid [TIBA], Panigrahi and Audus, 1966; for review, see Shimizu-Sato and Mori, 2001). In the 1930s, studies of bud outgrowth in plants with two decapitated shoots led Snow (1937) to suggest that auxin inhibits branching via a second messenger moving acropetally. Using radiolabeled indole-3-acetic acid (IAA), Hall and Hillman (1975) also proposed that auxin acts indirectly. Auxin was shown to move predo...

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Transport and metabolism of xylem cytokinins during lateral bud release in decapitated chickpea (Cicer arietinum) seedlings

Cited by 20 publications

References 44 publications

Roles for Auxin, Cytokinin, and Strigolactone in Regulating Shoot Branching

Roles for Auxin, Cytokinin, and Strigolactone in Regulating Shoot Branching

Conditional Auxin Response and Differential Cytokinin Profiles in Shoot Branching Mutants

Auxin Dynamics after Decapitation Are Not Correlated with the Initial Growth of Axillary Buds

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