<i>BRC1</i>expression regulates bud activation potential, but is not necessary or sufficient for bud growth inhibition in Arabidopsis

Seale, Madeleine; Bennett, Tom; Leyser, Ottoline

doi:10.1242/dev.145649

Cited by 110 publications

(121 citation statements)

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“…This effect of sugar on bud outgrowth through strigolactone pathway matches with the sucrose-mediated repression of MAX2 expression in rose buds (Barbier et al , 2015b) and the downregulation of MAX2 in response to defoliation and shade in sorghum (Kebrom et al , 2010). Moreover, in rose and pea, sucrose inhibited the expression of BRC1 (Mason et al , 2014; Barbier et al , 2015b), encoding a transcription factor inhibiting bud outgrowth (Aguilar-Martinez et al , 2007) and also involved in strigolactone signaling (Braun et al , 2012; Dun et al , 2012; Dun et al , 2013; Seale et al , 2017). Collectively, these findings prompt us to identify the molecular components of strigolactone signaling involved in sugar-mediated bud outgrowth promotion.…”

Section: Discussionmentioning

confidence: 99%

Sugar availability suppresses the auxin-induced strigolactone pathway to promote bud outgrowth

Bertheloot

Barbier

Boudon

et al. 2019

Preprint

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+33 (0)2 41 22 56 32 2 SUMMARY• Apical dominance occurs when the growing shoot tip inhibits the outgrowth of axillary buds. Apically-derived auxin in the nodal stem indirectly inhibits bud outgrowth via cytokinins and strigolactones. Recently, sugar deprivation was found to contribute to this phenomenon.• Using rose and pea, we investigated whether sugar availability interacts with auxin in bud outgrowth control, and the role of cytokinins and strigolactones, in vitro and in planta.• We show that sucrose antagonizes auxin's effect on bud outgrowth, in a dosedependent and coupled manner. Sucrose also suppresses strigolactone-inhibition of outgrowth, and rms3 strigolactone-perception mutant is less affected by reducing sucrose supply; however, sucrose does not interfere with the regulation of cytokinin levels by auxin, and stimulates outgrowth even with optimal cytokinin supply. These observations were assembled into a computational model where sucrose represses bud response to strigolactones, largely independently of cytokinin levels. It quantitatively captures our observed dose-dependent sucrose-hormones effects on bud outgrowth, and allows us to express outgrowth response to various combinations of auxin and sucrose levels as a simple quantitative law.• This study places sugars in the bud outgrowth regulatory network, and paves the way for better understanding of branching plasticity in response to environmental and genotypic factors.Versailles, France) for providing the seeds of Pisum sativum and GR24. We thank the Environment and Agronomy department of INRA for financial support.

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Section: Discussionmentioning

confidence: 99%

Sugar availability suppresses the auxin-induced strigolactone pathway to promote bud outgrowth

Bertheloot

Barbier

Boudon

et al. 2019

Preprint

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“…Strigolactones and cytokinins antagonistically regulate expression of the BRANCHED1 (BRC1) transcription factor (Aguilar‐Martínez et al ., ; Dun et al ., ), which is required to inhibit branching. The consensus view is that other genes and processes may yet be discovered to play a role in control of shoot branching (Aguilar‐Martínez et al ., ; Seale et al ., ).…”

Section: Introductionmentioning

confidence: 97%

Trehalose 6‐phosphate is involved in triggering axillary bud outgrowth in garden pea (Pisum sativum L.)

et al. 2017

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SUMMARYTrehalose 6-phosphate (Tre6P) is a signal of sucrose availability in plants, and has been implicated in the regulation of shoot branching by the abnormal branching phenotypes of Arabidopsis (Arabidopsis thaliana) and maize (Zea mays) mutants with altered Tre6P metabolism. Decapitation of garden pea (Pisum sativum) plants has been proposed to release the dormancy of axillary buds lower down the stem due to changes in sucrose supply, and we hypothesized that this response is mediated by Tre6P. Decapitation led to a rapid and sustained rise in Tre6P levels in axillary buds, coinciding with the onset of bud outgrowth. This response was suppressed by simultaneous defoliation that restricts the supply of sucrose to axillary buds in decapitated plants. Decapitation also led to a rise in amino acid levels in buds, but a fall in phosphoenolpyruvate and 2-oxoglutarate. Supplying sucrose to stem node explants in vitro triggered a concentration-dependent increase in the Tre6P content of the buds that was highly correlated with their rate of outgrowth. These data show that changes in bud Tre6P levels are correlated with initiation of bud outgrowth following decapitation, suggesting that Tre6P is involved in the release of bud dormancy by sucrose. Tre6P might also be linked to a reconfiguration of carbon and nitrogen metabolism to support the subsequent growth of the bud into a new shoot.

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“…Though BRC1 and PIN1 are important targets of SL, their actions do not entirely explain the inhibition of branching by SL. BRC1 expression is not always correlated with bud inhibition (Arite et al, 2007;Seale et al, 2017), and preventing auxin transport out of buds using an auxin transport inhibitor, 1-N-Naphthylphthalamic acid (NPA), does not inhibit early bud growth (Brewer et al, 2009;Brewer et al, 2015;Chabikwa et al, 2019). This indicates the possibility that other targets of SL are yet to be discovered.…”

Section: Introductionmentioning

confidence: 99%

Hormonal regulation of the BRC1-dependent strigolactone transcriptome involved in shoot branching responses

Kerr

Germain

et al. 2020

Preprint

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The plant hormone strigolactone (SL) inhibits shoot branching by suppressing the growth of axillary buds. This is thought to occur largely via regulation of the transcription factor BRANCHED1 (BRC1). Here, we clarify the central role of BRC1 and identify additional transcriptional responses by which SL might regulate axillary bud outgrowth in garden pea (Pisum sativum). We used a transcriptomic approach to identify differentially expressed transcripts in pea axillary buds in response to a synthetic SL, rac-GR24. Changes in transcript abundance were confirmed by measuring their response to GR245DS. BRC1 was required for the regulation of over half of the fourteen GR245DS-regulated genes, confirming its role as a mediator of SL transcriptional responses in axillary buds. All, but one, of the BRC1-dependent GR245DS-regulated genes were also regulated by branch-promoting treatments cytokinin (CK) and/or decapitation in an opposing manner to SL. This suggests that SL, CK, and decapitation regulate shoot branching via a common pathway. We used correlational analyses of gene co-expression data to infer a gene regulatory network consisting of nine key co-expression modules correlated with rac-GR24 treatment. Enrichment of GO terms such as cell proliferation, carbohydrate responses, and abscisic acid and jasmonic acid hormone pathways suggest a role for these in SL-mediated inhibition of shoot branching. In summary, we have shown that BRC1 is indeed a key transcriptional regulator of the SL signalling pathway in pea buds as well as a focal point of the SL, CK and decapitation signalling pathways to coordinate shoot branching in pea buds.One Sentence SummaryIdentification of genes that are strigolactone-responsive and BRC1-dependent in pea buds reveals a high degree of overlap among strigolactone, cytokinin and decapitation response pathways.

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BRC1expression regulates bud activation potential, but is not necessary or sufficient for bud growth inhibition in Arabidopsis

Cited by 110 publications

References 69 publications

Sugar availability suppresses the auxin-induced strigolactone pathway to promote bud outgrowth

Sugar availability suppresses the auxin-induced strigolactone pathway to promote bud outgrowth

Trehalose 6‐phosphate is involved in triggering axillary bud outgrowth in garden pea (Pisum sativum L.)

Hormonal regulation of the BRC1-dependent strigolactone transcriptome involved in shoot branching responses

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