Cortical microtubule remodelling during strigolactone- and light-mediated growth inhibition of Arabidopsis hypocotyls

Strigolactones are phytohormones involved in shoot branching and hypocotyl elongation. The latter phenomenon was addressed herein by the exogenous application of a synthetic strigolactone GR24 and an inhibitor of strigolactone biosynthesis TIS108 on hypocotyls of wild type Arabidopsis and a strigolactone signalling mutant max2-1 (more axillary growth 2-1). Owing to the interdependence between light and strigolactone signalling, the present work was extended to seedling cultivation under a standard light/dark regime, or under continuous darkness. Given the essential role of the cortical microtubules in cell elongation, their organization and dynamics were characterized under the conditions of altered strigolactone signalling using fluorescence microscopy methods with different spatiotemporal capacities such as confocal laser scanning microscopy and structured illumination microscopy. It was found that the strigolactone-dependent inhibition of hypocotyl elongation correlated with changes in cortical microtubule organization and dynamics, visualized in living wild type and max2-1 seedlings stably expressing genetically-encoded fluorescent molecular markers for microtubules. Quantitative analysis of microscopic datasets revealed that chemical and/or genetic manipulation of strigolactone signalling affected microtubule remodelling, especially under light conditions. The application of GR24 and TIS108 in dark conditions partially alleviated cytoskeletal rearrangement, suggesting a new mechanistic connection between the cytoskeletal behaviour and the light-dependence of strigolactone signalling.HighlightStrigolactones regulate organization and dynamics of cortical microtubules in hypocotyl cells, which contributes to the light-mediated inhibition of hypocotyl growth in Arabidopsis seedlings.

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

Shoot branching, which is regulated by a complex signalling network, is a major component of plant architecture and therefore of crop yield. Sugars, acting in a network with hormones, have recently emerged as key players in the control of shoot branching. Previous studies in dicotyledonous plants have shown that sucrose suppresses the inhibitory effect of the plant hormone strigolactone (SL) during this process. The molecular mechanisms underlying this effect are unknown. Here we show that sucrose could antagonise the suppressive action of SL on tillering in rice. At the mechanistic level, we revealed that sucrose alleviates SL-mediated degradation of D53. Increase in sucrose availability inhibits the expression of D3, which encodes the orthologue of the arabidopsis F-box MAX2 required for SL signalling. Over-expression of D3 prevented sucrose from inhibiting D53 degradation and enabled the SL inhibition of tillering under high sucrose. The enhanced bud elongation of the d3 mutant to sucrose treatment indicates that suppressed SL perception reduces the minimum amount of sucrose required for sustained bud outgrowth. Decapitation and sugar feeding experiments in pea indicate that RMS4, the D3/MAX2 orthologue in pea, is also involved in the interactions between sucrose and SL. This work shows that D3/MAX2/RMS4 is a key component in the integrating both SL and sugar pathways during the regulation of shoot architecture.

HEXOKINASE1 interferes with cytokinin synthesis and strigolactone perception during sugar-induced shoot branching

ABSTRACT-Plant architecture is controlled by several endogenous signals including hormones and sugars. However, only little is known about the nature and roles of the sugar signalling pathways in this process. Here we test whether the sugar pathway mediated by HEXOKINASE1 (HXK1) is involved in the control of shoot branching.-To test the involvement of HXK1 in the control of shoot architecture we modulated the HXK1 pathway using physiological and genetic approaches in diverse plants, rose, arabidopsis and pea and evaluated impacts of hormonal pathways.-We show that triggering a hexokinase-dependent pathway was able to promote bud outgrowth in pea and rose. In arabidopsis, both HXK1 deficiency and defoliation led to decreased shoot branching and conferred hypersensitivity to auxin. HXK1 expression was positively correlated with sugar availability. HXK1-deficient plants displayed decreased cytokinin levels and increased expression of MAX2 which is required for strigolactone signalling. The branching phenotype of HXK1-deficient plants could be partly restored by cytokinin treatment and strigolactone deficiency could override the negative impact of HXK1 deficiency on shoot branching.-Our observations demonstrate that a HXK1-dependent pathway contributes to the regulation of shoot branching and interact with hormones to modulate plant architecture.