Suppression of Tiller Bud Activity in Tillering Dwarf Mutants of Rice

Ishikawa, Satoshi; Maekawa, Masahiko; Arite, Tomotsugu; Onishi, Kazumitsu; Takamure, Itsuro; Kyozuka, Junko

doi:10.1093/pcp/pci022

Cited by 468 publications

(388 citation statements)

References 30 publications

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“…Extensive genetic studies in Arabidopsis, pea, and rice using SL-deficient and -insensitive mutants have identified components of a conserved SL signaling pathway [8][9][10][11][12][13], including rice dwarf 14 (d14) and dwarf 3 (d3). Due to the homology between D3 and the auxin and jasmonate receptors, TIR1 and COI1, and between D14 and the gibberellin receptor GID1 and the putative karrikin receptor KAI2, it had been speculated that both D3 and D14 could be candidates for the SL receptor [14].…”

Section: Introductionmentioning

confidence: 99%

Destabilization of strigolactone receptor DWARF14 by binding of ligand and E3-ligase signaling effector DWARF3

et al. 2015

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Strigolactones (SLs) are endogenous hormones and exuded signaling molecules in plant responses to low levels of mineral nutrients. Key mediators of the SL signaling pathway in rice include the α/β-fold hydrolase DWARF 14 (D14) and the F-box component DWARF 3 (D3) of the ubiquitin ligase SCF D3 that mediate ligand-dependent degradation of downstream signaling repressors. One perplexing feature is that D14 not only functions as the SL receptor but is also an active enzyme that slowly hydrolyzes diverse natural and synthetic SLs including GR24, preventing the crystallization of a binary complex of D14 with an intact SL as well as the ternary D14/SL/D3 complex. Here we overcome these barriers to derive a structural model of D14 bound to intact GR24 and identify the interface that is required for GR24-mediated D14-D3 interaction. The mode of GR24-mediated signaling, including ligand recognition, hydrolysis by D14, and ligand-mediated D14-D3 interaction, is conserved in structurally diverse SLs. More importantly, D14 is destabilized upon the binding of ligands and D3, thus revealing an unusual mechanism of SL recognition and signaling, in which the hormone, the receptor, and the downstream effectors are systematically destabilized during the signal transduction process.

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Section: Introductionmentioning

confidence: 99%

Destabilization of strigolactone receptor DWARF14 by binding of ligand and E3-ligase signaling effector DWARF3

et al. 2015

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“…Recent studies on a series of branching mutants, such as more axillary growth (max) of Arabidopsis [37][38][39][40], ramosus (rms) mutants of pea [41][42][43], decreased apical dominance (dad) mutants of petunia [44,45] and dwarf (d) mutants of rice [46][47][48][49][50][51], have revealed strigolactone as a second messenger of auxin action on the control of AM outgrowth [52,53]. Strigolactones, a group of terpenoid lactones that have been found in root exudates of diverse plant species, are synthesized from carotenoids in roots and transported acropetally or synthesized locally to repress the outgrowth of shoot branches [38,[54][55][56].…”

Section: Introductionmentioning

confidence: 99%

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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“…Paradoxically, the mutants were found to have generally higher levels of auxin and lower levels of xylem cytokinin, facts difficult to reconcile with ideas about the roles of auxin and cytokinin in regulating bud outgrowth (Beveridge et al, 1997). These mutants were ramosus (rms) in pea (Pisum sativum), decreased apical dominance (dad) in petunia (Petunia hybrida), more axillary growth (max) in Arabidopsis (Arabidopsis thaliana), and particular dwarf (d) mutants in rice (Oryza sativa; Beveridge et al, 1994;Napoli, 1996;Stirnberg et al, 2002;Ishikawa et al, 2005). Grafting studies demonstrated that increased bud outgrowth in some of the mutants was caused by the loss of a long-distance mobile signal (termed SMS; Beveridge, 2006) that moved upward from lower tissues (Beveridge et al, 1994;Napoli, 1996;Foo et al, 2001;Turnbull et al, 2002).…”

mentioning

confidence: 99%

“…Likewise, RMS5, MAX3, and D17/HTD1 were found to encode CCD7 (Booker et al, 2004;Johnson et al, 2006;Zou et al, 2006). In contrast, the SMS response mutants, max2, rms4, and d3, were found to be mutated in an orthologous gene encoding an F-box protein (Stirnberg et al, 2002;Ishikawa et al, 2005;Johnson et al, 2006). Recently, the testing of putative carotenoidderived compounds led to the discovery that SMS is a strigolactone or downstream product (Gomez-Roldan et al, 2008;Umehara et al, 2008).…”

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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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Suppression of Tiller Bud Activity in Tillering Dwarf Mutants of Rice

Cited by 468 publications

References 30 publications

Destabilization of strigolactone receptor DWARF14 by binding of ligand and E3-ligase signaling effector DWARF3

Destabilization of strigolactone receptor DWARF14 by binding of ligand and E3-ligase signaling effector DWARF3

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

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

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