Sucrose promotes D53 accumulation and tillering in rice

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.