Control of axillary bud initiation and shoot architecture in <i>Arabidopsis</i> through the <i>SUPERSHOOT</i> gene

Tantikanjana, Titima; Yong, Jean Wan Hong; Letham, D. S.; Griffith, Megan; Hussain, Mumtaz; Ljung, Karin; Sandberg, Göran; Sundaresan, Venkatesan

doi:10.1101/gad.887301

Cited by 181 publications

(170 citation statements)

References 60 publications

(67 reference statements)

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confidence: 88%

“…These mutants exhibit massive proliferation of shoots, together with other developmental defects. The quantification of hormone levels in sps/cyp79F1 mutant plants indicates that both auxin and cytokinins are higher in the mutants, but the phenotypes of the sps/cyp79F1 plants are consistent with higher levels of cytokinins rather than auxins as the key factor responsible for the change in branching pattern (Tantikanjana et al, 2001).Despite the fact that sps/cyp79F1 plants resemble hormone mutants, biochemical studies have shown that SPS/CYP79F1 gene encodes an enzyme catalyzing metabolism of both short-chain and long-chain elongated Met-derivatives in the biosynthesis of aliphatic glucosinolates (Hansen et al, 2001;Chen et al, 2003). Glucosinolates are a group of secondary plant metabolites known to play a role in plant defense and are sources of flavor compounds, cancer-preventing agents, and bioherbicides.…”

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confidence: 89%

“…The two plant hormones not only play opposite roles in controlling plant growth and development, but also influence each other hormone homeostasis (Binns et al, 1987;Palni et al, 1988;Bangerth, 1994;Zhang et al, 1995;Makarova et al, 1996). We and others have described Arabidopsis mutants called supershoot (sps) or bushy (bus), which are disrupted in the gene encoding the cytochrome P450 CYP79F1 (Reintanz et al, 2001;Tantikanjana et al, 2001). These mutants exhibit massive proliferation of shoots, together with other developmental defects.…”

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Functional Analysis of the Tandem-Duplicated P450 Genes SPS/BUS/CYP79F1 and CYP79F2 in Glucosinolate Biosynthesis and Plant Development by Ds Transposition-Generated Double Mutants

et al. 2004

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A significant fraction (approximately 17%) of Arabidopsis genes are members of tandemly repeated families and pose a particular challenge for functional studies. We have used the Ac-Ds transposition system to generate single-and doubleknockout mutants of two tandemly duplicated cytochrome P450 genes, SPS/BUS/CYP79F1 and CYP79F2. We have previously described the Arabidopsis supershoot mutants in CYP79F1 that exhibit massive overproliferation of shoots. Here we use a cytokinin-responsive reporter ARR5::uidA and an auxin-responsive reporter DR5::uidA in the sps/cyp79F1 mutant to show that increased levels of cytokinin, but not auxin, correlate well with the expression pattern of the SPS/CYP79F1 gene, supporting the involvement of this gene in cytokinin homeostasis. Further, we isolated Ds gene trap insertions in the CYP79F2 gene, and find these mutants to be defective mainly in the root system, consistent with a root-specific expression pattern. Finally, we generated double mutants in CYP79F1 and CYP79F2 using secondary transpositions, and demonstrate that the phenotypes are additive. Previous biochemical studies have suggested partially redundant functions for SPS/CYP79F1 and CYP79F2 in aliphatic glucosinolate synthesis. Our analysis shows that aliphatic glucosinolate biosynthesis is completely abolished in the double-knockout plants, providing genetic proof for the proposed biochemical functions of these genes. This study also provides further demonstration of how gluconisolate biosynthesis, regarded as secondary metabolism, is intricately linked with hormone homeostatis and hence with plant growth and development.Plant growth and development requires coordination of networks of biological processes within the plant, as well as with responses to external environments. The control of shoot branching by auxin and cytokinin is a well-known example of hormone interactions in controlling plant development. Cytokinin plays a key role in promoting bud growth, whereas auxin has an inhibitory effect. Therefore, the outcome appears to depend on the ratio of the two hormones (for review, see Tamas, 1995;Li and Bangerth, 1992). The two plant hormones not only play opposite roles in controlling plant growth and development, but also influence each other hormone homeostasis (Binns et al., 1987;Palni et al., 1988;Bangerth, 1994;Zhang et al., 1995;Makarova et al., 1996). We and others have described Arabidopsis mutants called supershoot (sps) or bushy (bus), which are disrupted in the gene encoding the cytochrome P450 CYP79F1 (Reintanz et al., 2001;Tantikanjana et al., 2001). These mutants exhibit massive proliferation of shoots, together with other developmental defects. The quantification of hormone levels in sps/cyp79F1 mutant plants indicates that both auxin and cytokinins are higher in the mutants, but the phenotypes of the sps/cyp79F1 plants are consistent with higher levels of cytokinins rather than auxins as the key factor responsible for the change in branching pattern (Tantikanjana et al., 2001).Despite the fact that s...

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confidence: 89%

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confidence: 99%

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Functional Analysis of the Tandem-Duplicated P450 Genes SPS/BUS/CYP79F1 and CYP79F2 in Glucosinolate Biosynthesis and Plant Development by Ds Transposition-Generated Double Mutants

et al. 2004

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“…The outgrowth phenotype of the bud2 axillary buds may also result from altered cytokinin biosynthesis and/ or response, because cytokinin has long been proposed as a secondary messenger of IAA in controlling shoot branching [63][64][65]. We therefore compared the endogenous levels of various cytokinins between bud2-2 and wild-type seedlings.…”

Section: Altered Biosynthesis Of Cytokinins In Bud2 Plantsmentioning

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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“…Until the isolation and characterization of branching mutants in various species, it was not possible to address these issues. In recent decades, many branching mutants have been isolated that have problems with auxin, cytokinin, or brassinosteroids, for example, and show highly pleiotropic phenotypes typical for these hormones (Lincoln et al, 1990;Azpiroz et al, 1998;Tantikanjana et al, 2001). However, a class of mutants were isolated that displayed a specific increase in bud outgrowth that was not correlated with any known hormonal signal (Beveridge et al, 1996(Beveridge et al, , 1997.…”

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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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Control of axillary bud initiation and shoot architecture in Arabidopsis through the SUPERSHOOT gene

Cited by 181 publications

References 60 publications

Functional Analysis of the Tandem-Duplicated P450 Genes SPS/BUS/CYP79F1 and CYP79F2 in Glucosinolate Biosynthesis and Plant Development by Ds Transposition-Generated Double Mutants

Functional Analysis of the Tandem-Duplicated P450 Genes SPS/BUS/CYP79F1 and CYP79F2 in Glucosinolate Biosynthesis and Plant Development by Ds Transposition-Generated Double Mutants

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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