SLR1 inhibits MOC1 degradation to coordinate tiller number and plant height in rice

Zhigang Liao,Liquan Kou,Xiangbing Meng,Guifu Liu,Hong Yu,Jingbo Duan,Kun Yuan,Mingjiang Chen,Jiayang Li,Yanhui Jing,Steven M Smith,Chaoji Yu

doi:10.1038/s41467-019-10667-2

Abstract

The breeding of cereals with altered gibberellin (GA) signaling propelled the ‘Green Revolution’ by generating semidwarf plants with increased tiller number. The mechanism by which GAs promote shoot height has been studied extensively, but it is not known what causes the inverse relationship between plant height and tiller number. Here we show that rice tiller number regulator MONOCULM 1 (MOC1) is protected from degradation by binding to the DELLA protein SLENDER RICE 1 (SLR1). GAs trigger the degradation of SLR1, leading to stem elongation and also to the degradation of MOC1, and hence a decrease in tiller number. This discovery provides a molecular explanation for the coordinated control of plant height and tiller number in rice by GAs, SLR1 and MOC1.

Highlights

The breeding of cereals with altered gibberellin (GA) signaling propelled the ‘Green Revolution’ by generating semidwarf plants with increased tiller number
We found that GAdeficient or GA-signaling mutants, including semidwarf 1, a GA biosynthesis mutant defective in GA20ox-2, sdg, and slr1-d1, a GA-signaling mutant, produced more tillers and had a shorter stature than the WT plants (Fig. 1a–c; Supplementary Fig. 2a–f)
We propose a model to illustrate how GA signaling via SLENDER RICE 1 (SLR1) directly coordinates plant height and tiller number (Fig. 5j)

Summary

Introduction

The breeding of cereals with altered gibberellin (GA) signaling propelled the ‘Green Revolution’ by generating semidwarf plants with increased tiller number. 1234567890():,; Tiller number and plant height are two important factors determining cereal plant architecture and grain yield[1]. Among the genes involved in determining tiller number in rice, MOC1 is one of the most important because it is required for the formation of axillary meristems (AM) and subsequent bud outgrowth[1,13]. Overexpressing plants are associated with an increased number of axillary buds and tillers[13]. Double-mutant analyses suggest that MOC1, LAX1, and LAX2 function in partially independent but overlapping pathways to regulate AM establishment and maintenance[19]. Phytohormones are another class of important factors determining bud fate. It has long been known that auxin inhibits the outgrowth of axillary buds, whereas cytokinin (CK) stimulates[21]

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