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Bertheloot, J.

Publications and source records attributed to Bertheloot, J..

3 recordsLinked to original sources

Branching Varies with Light Limitation Scenarios in relation with Changes in Carbon Source-Sink Dynamics.

Bud outgrowth is a major component of plant architectural plasticity and is influenced by light conditions. While the inhibitory effect of low light intensity on branching is well documented, the underlying regulators remain debated and, especially, the role of sugar availability has never been thoroughly evaluated. Here, we combined experiments with a computational approach quantifying carbon source-sink balance in single-axis rose plants to investigate how continuous and transient light limitation regulate bud outgrowth. Continuous low light reduced photosynthesis, leading to decreased sugar availability and inhibited bud outgrowth. In contrast, a transient period of low light followed by high light unexpectedly stimulated bud outgrowth, shortened the delay between outgrowth of successive buds, and produced an over-branched phenotype. This response resulted from a non-reversible reduction in the growth of apical organs appearing under low light, which lowered carbon demand and caused sugar over-accumulation after the return to high light. Manipulating carbon supply and demand through leaf masking, photosynthetic inhibition, and targeted sucrose feeding causally confirmed the central role of sugar availability in these contrasting responses. Beyond these findings, key requirements for models simulating branching plasticity were identified and this work provides a basis for predicting branching responses under fluctuating and complex light environments. HighlightBud outgrowth, a key component of plant plasticity, is regulated by light intensity through sugar availability. Continuous and transient low light have opposite effects by limiting sugar production and use, respectively.

plant biology↗

Sucrose represses the expression of the strigolactone signalling gene D3/RMS4/MAX2 to promote tillering

- 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.

plant biology↗

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

O_LIApical 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.\nC_LIO_LIUsing 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.\nC_LIO_LIWe show that sucrose antagonizes auxins 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.\nC_LIO_LIThis 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.\nC_LI

plant biology↗