Auxin Acts in Xylem-Associated or Medullary Cells to Mediate Apical Dominance

Booker, Jonathan; Chatfield, Steven P.; Leyser, Ottoline

doi:10.1105/tpc.007542

Cited by 193 publications

(131 citation statements)

References 76 publications

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“…However, unraveling the action of apically derived auxin has been challenging, mainly because auxin was found to move strictly downward in the vascular cambium of the stem (the polar auxin transport stream) and apparently cannot change direction to move upward to enter axillary buds and branches (Snow, 1937;Hall and Hillman, 1975;Morris, 1977;Morris and Thomas, 1978;Bangerth, 1989;Prasad et al, 1993;Booker et al, 2003). In addition, while apically derived auxin moved downward through live cells (Morris and Thomas, 1978), the inhibiting influence was able to be transmitted upward through dead tissue (Snow, 1929).…”

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confidence: 99%

Strigolactone Acts Downstream of Auxin to Regulate Bud Outgrowth in Pea and Arabidopsis

et al. 2009

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During the last century, two key hypotheses have been proposed to explain apical dominance in plants: auxin promotes the production of a second messenger that moves up into buds to repress their outgrowth, and auxin saturation in the stem inhibits auxin transport from buds, thereby inhibiting bud outgrowth. The recent discovery of strigolactone as the novel shootbranching inhibitor allowed us to test its mode of action in relation to these hypotheses. We found that exogenously applied strigolactone inhibited bud outgrowth in pea (Pisum sativum) even when auxin was depleted after decapitation. We also found that strigolactone application reduced branching in Arabidopsis (Arabidopsis thaliana) auxin response mutants, suggesting that auxin may act through strigolactones to facilitate apical dominance. Moreover, strigolactone application to tiny buds of mutant or decapitated pea plants rapidly stopped outgrowth, in contrast to applying N-1-naphthylphthalamic acid (NPA), an auxin transport inhibitor, which significantly slowed growth only after several days. Whereas strigolactone or NPA applied to growing buds reduced bud length, only NPA blocked auxin transport in the bud. Wild-type and strigolactone biosynthesis mutant pea and Arabidopsis shoots were capable of instantly transporting additional amounts of auxin in excess of endogenous levels, contrary to predictions of auxin transport models. These data suggest that strigolactone does not act primarily by affecting auxin transport from buds. Rather, the primary repressor of bud outgrowth appears to be the auxindependent production of strigolactones.

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Strigolactone Acts Downstream of Auxin to Regulate Bud Outgrowth in Pea and Arabidopsis

et al. 2009

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“…It is transported along the shoot-root axis from cell to cell in a polar manner, which is essential for inhibiting the outgrowth of axillary buds Leyser, 2003;Sieberer and Leyser, 2006). However, a large body of evidence suggests that auxin cannot directly enter the axillary buds and that a second messenger is required to inhibit the outgrowth of axillary buds (Shelagh and John, 1975;Morris, 1977;Pilate et al, 1989;Prasad et al, 1993;Booker et al, 2003). Cytokinin is the first reported second messenger candidate, which is synthesized in roots and transported acropetally in the xylem to promote directly the outgrowth of axillary buds (Van Dijck et al, 1988;Cline, 1991;Eklof et al, 1997;Kapchina-Toteva et al, 2000;Nordstrom et al, 2004).…”

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confidence: 99%

DWARF27, an Iron-Containing Protein Required for the Biosynthesis of Strigolactones, Regulates Rice Tiller Bud Outgrowth

et al. 2009

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Tillering in rice (Oryza sativa) is one of the most important agronomic traits that determine grain yields. Previous studies on rice tillering mutants have shown that the outgrowth of tiller buds in rice is regulated by a carotenoid-derived MAX/RMS/D (more axillary branching) pathway, which may be conserved in higher plants. Strigolactones, a group of terpenoid lactones, have been recently identified as products of the MAX/RMS/D pathway that inhibits axillary bud outgrowth. We report here the molecular genetic characterization of d27, a classic rice mutant exhibiting increased tillers and reduced plant height. D27 encodes a novel iron-containing protein that localizes in chloroplasts and is expressed mainly in vascular cells of shoots and roots. The phenotype of d27 is correlated with enhanced polar auxin transport. The phenotypes of the d27 d10 double mutant are similar to those of d10, a mutant defective in the ortholog of MAX4/RMS1 in rice. In addition, 29-epi-5-deoxystrigol, an identified strigolactone in root exudates of rice seedlings, was undetectable in d27, and the phenotypes of d27 could be rescued by supplementation with GR24, a synthetic strigolactone analog. Our results demonstrate that D27 is involved in the MAX/RMS/D pathway, in which D27 acts as a new member participating in the biosynthesis of strigolactones.

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“…Auxin was first regarded as a direct regulator in this process [14], a notion strengthened thereafter by physiological studies on decapitated shoot apices [15][16][17], and by analyzing auxin biosynthesis, transport and signaling [18][19][20][21][22][23][24][25][26][27][28][29] in plants. However, when radiolabelled auxin was applied to a decapitated stump, the outgrowth of axillary buds was inhibited even though radiolabelled auxin was not found to accumulate in axillary buds, suggesting an indirect suppression effect of auxin on the AM outgrowth [28,30] and the presence of second messengers.Cytokinin has been proposed as a second messenger that mediates the action of auxin in controlling the apical dominance, because it promotes the outgrowth of lateral buds when directly applied to buds [31]. Although an antagonistic role of auxin and cytokinin in the regulation of apical dominance has been postulated for decades, little is known about the underlying molecular mechanisms.…”

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The BUD2 mutation affects plant architecture through altering cytokinin and auxin responses in Arabidopsis

et al. 2010

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The ratio of auxin and cytokinin plays a crucial role in regulating aerial architecture by promoting or repressing axillary bud outgrowth. We have previously identified an Arabidopsis mutant bud2 that displays altered root and shoot architecture, which results from the loss-of-function of S-adenosylmethionine decarboxylase 4 (SAMDC4). In this study, we demonstrate that BUD2 could be induced by auxin, and the induction is dependent on auxin signaling. The mutation of BUD2 results in hyposensitivity to auxin and hypersensitivity to cytokinin, which is confirmed by callus induction assays. Our study suggests that polyamines may play their roles in regulating the plant architecture through affecting the homeostasis of cytokinins and sensitivities to auxin and cytokinin. IntroductionPolyamines, including diamine putrescine, triamine spermidine and tetraamine spermine, are low-molecularmass organic cations. They exist widely in all living organisms and are essential for their survival, because blocking of the biosynthesis of polyamines leads to lethal phenotypes in animals [1] and higher plants [2][3][4]. In higher plants, polyamines have been proposed to function in response to environmental stresses and in regulating growth and development [4][5][6][7][8][9][10][11]. Plant molecular and physiological studies over past decades have shown that higher plants defective in producing polyamines often have altered plant architecture, with reduced plant height or more branches in shoots and roots [4,[10][11][12][13]. However, the underlying mechanisms still remain largely elusive.Branches of higher plants originate from the axillary meristems (AMs) of shoots, and formation of a branch generally consists of the initiation of a new AM and its subsequent outgrowth. However, an AM may arrest its growth under some conditions, forming a dormant bud. The dormant buds will release their outgrowth once they sense a permissible environmental or developmental signal. In many plant species, axillary buds become dormant due to the inhibiting effects of the primary shoot apex on the outgrowth of AMs, a phenomenon known as 'apical dominance'. Auxin was first regarded as a direct regulator in this process [14], a notion strengthened thereafter by physiological studies on decapitated shoot apices [15][16][17], and by analyzing auxin biosynthesis, transport and signaling [18][19][20][21][22][23][24][25][26][27][28][29] in plants. However, when radiolabelled auxin was applied to a decapitated stump, the outgrowth of axillary buds was inhibited even though radiolabelled auxin was not found to accumulate in axillary buds, suggesting an indirect suppression effect of auxin on the AM outgrowth [28,30] and the presence of second messengers.Cytokinin has been proposed as a second messenger that mediates the action of auxin in controlling the apical dominance, because it promotes the outgrowth of lateral buds when directly applied to buds [31]. Although an antagonistic role of auxin and cytokinin in the regulation of apical dominance has been postu...

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Auxin Acts in Xylem-Associated or Medullary Cells to Mediate Apical Dominance

Cited by 193 publications

References 76 publications

Strigolactone Acts Downstream of Auxin to Regulate Bud Outgrowth in Pea and Arabidopsis

Strigolactone Acts Downstream of Auxin to Regulate Bud Outgrowth in Pea and Arabidopsis

DWARF27, an Iron-Containing Protein Required for the Biosynthesis of Strigolactones, Regulates Rice Tiller Bud Outgrowth

The BUD2 mutation affects plant architecture through altering cytokinin and auxin responses in Arabidopsis

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