ORCID Profile
0000-0001-5941-2227
Current Organisation
INRA Centre Angers-Nantes
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Publisher: Wiley
Date: 20-10-2019
DOI: 10.1111/NPH.16201
Abstract: 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 antagonises auxin's effect on bud outgrowth, in a dose-dependent and coupled manner. Sucrose also suppresses strigolactone inhibition of outgrowth and the 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 in which 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 a better understanding of branching plasticity in response to environmental and genotypic factors.
Publisher: Wiley
Date: 30-11-2022
DOI: 10.1111/NPH.17834
Abstract: Shoot branching is regulated by multiple signals. Previous studies have indicated that sucrose may promote shoot branching through suppressing the inhibitory effect of the hormone strigolactone (SL). However, the molecular mechanisms underlying this effect are unknown. Here, we used molecular and genetic tools to identify the molecular targets underlying the antagonistic interaction between sucrose and SL. We showed that sucrose antagonizes the suppressive action of SL on tillering in rice and on the degradation of D53, a major target of SL signalling. Sucrose inhibits the gene expression of D3 , the orthologue of the Arabidopsis F‐box MAX2 required for SL signalling. Overexpression of D3 antagonizes sucrose inhibition of D53 degradation and enables the SL inhibition of tillering under high sucrose. Sucrose prevents SL‐induced degradation of D14, the SL receptor involved in D53 degradation. In contrast to D3 , D14 overexpression enhances D53 protein levels and sucrose‐induced tillering, even in the presence of SL. Our results show that sucrose inhibits SL response by affecting key components of SL signalling and, together with previous studies reporting the inhibition of SL synthesis by nitrate and phosphate, demonstrate the central role played by SLs in the regulation of plant architecture by nutrients.
Publisher: Oxford University Press (OUP)
Date: 13-04-2015
DOI: 10.1093/JXB/ERV047
Publisher: Oxford University Press (OUP)
Date: 05-02-2021
DOI: 10.1093/JXB/ERAB046
Abstract: Shoot branching is a pivotal process during plant growth and development, and is antagonistically orchestrated by auxin and sugars. In contrast to extensive investigations on hormonal regulatory networks, our current knowledge on the role of sugar signalling pathways in bud outgrowth is scarce. Based on a comprehensive stepwise strategy, we investigated the role of glycolysis/the tricarboxylic acid (TCA) cycle and the oxidative pentose phosphate pathway (OPPP) in the control of bud outgrowth. We demonstrated that these pathways are necessary for bud outgrowth promotion upon plant decapitation and in response to sugar availability. They are also targets of the antagonistic crosstalk between auxin and sugar availability. The two pathways act synergistically to down-regulate the expression of BRC1, a conserved inhibitor of shoot branching. Using Rosa calluses stably transformed with GFP-fused promoter sequences of RhBRC1 (pRhBRC1), glycolysis/TCA cycle and the OPPP were found to repress the transcriptional activity of pRhBRC1 cooperatively. Glycolysis/TCA cycle- and OPPP-dependent regulations involve the –1973/–1611 bp and –1206/–709 bp regions of pRhBRC1, respectively. Our findings indicate that glycolysis/TCA cycle and the OPPP are integrative parts of shoot branching control and can link endogenous factors to the developmental programme of bud outgrowth, likely through two distinct mechanisms.
Publisher: Cold Spring Harbor Laboratory
Date: 30-08-2019
DOI: 10.1101/752147
Abstract: 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 dose-dependent 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.
Publisher: Cold Spring Harbor Laboratory
Date: 11-11-2020
DOI: 10.1101/2020.11.10.377549
Abstract: - Shoot branching, a major component of shoot architecture, is regulated by multiple signals. Previous studies have indicated that sucrose may promote branching through suppressing the inhibitory effect of the hormone strigolactone (SL). However, the molecular mechanisms underlying this effect are unknown. - Here we used molecular and genetic tools to identify the molecular targets underlying the antagonistic interaction between sucrose and SL. - We showed that sucrose antagonises the suppressive action of SL on tillering in rice and on the degradation of D53, a major target of SL signalling. Sucrose inhibits the expression of D3 , the orthologue of the arabidopsis F-box protein MAX2 required for SL signalling. Over-expression of D3 prevents sucrose from inhibiting D53 degradation and enabled the SL inhibition of tillering under high sucrose. Sucrose also prevents SL-induced degradation of D14, the SL receptor involved in D53 degradation. Interestingly, D14 over-expression enhances D53 protein levels and sucrose-induced tillering. - Our results show that sucrose inhibits SL perception by targeting key components of SL signalling and, together with previous studies reporting the inhibition of SL synthesis by nitrate and phosphate, demonstrate the central role played by strigolactones in the regulation of plant architecture by nutrients.
No related grants have been discovered for Jessica Bertheloot.