An SPX-RLI1 Module Regulates Leaf Inclination in Response to Phosphate Availability in Rice

Leaf erectness is one of the key traits of plant architecture; in grains, plants with upright leaves can be planted close together, thus benefiting yield/unit area. Many factors, such as hormones, affect leaf inclination; however, how nutrition status, in particular phosphate (Pi) availability, affects leaf inclination remains largely unexplained. Here, we show that in rice (Oryza sativa), Pi deficiency stress inhibits lamina joint cell elongation, thus restricting lamina joint size and inducing leaf erectness in rice. The Pi starvationinduced proteins SPX1 (for Syg1/Pho81/XPR1) and SPX2 play a negative role in the regulation of leaf inclination. We further identified an SPX1-interacting protein, REGULATOR OF LEAF INCLINATION1 (RLI1), which positively regulates leaf inclination by affecting lamina joint cell elongation in rice. The rli1 mutants showed reduced leaf inclination and the RLI1 overexpressors showed increased leaf inclination. RLI1 directly activates the downstream genes BRASSINOSTEROID UPREGULATED1 (BU1) and BU1-LIKE 1 COMPLEX1 to control elongation of the lamina joint cells, therefore enhancing leaf inclination. We also found that Pi deficiency repressed the expression of RLI1. SPX1 protein interacts directly with RLI1, which could prevent RLI1 binding to the promoters of downstream genes. Therefore, SPX and RLI1 form a module to regulate leaf inclination in response to external Pi availability in rice.

叶片直立性是植物株型的关键性状之一；在谷类作物中，叶片直立的植株可以密植，从而有利于单位面积产量。许多因素，如激素，会影响叶片倾斜度；然而，营养状况，特别是磷酸盐（Pi）的有效性如何影响叶片倾斜度在很大程度上仍未得到解释。在此，我们表明在水稻（Oryza sativa）中，缺磷胁迫会抑制叶枕细胞伸长，从而限制叶枕大小并诱导水稻叶片直立。缺磷诱导的蛋白质SPX1（Syg1/Pho81/XPR1的缩写）和SPX2在叶片倾斜度的调控中起负作用。我们进一步鉴定了一种与SPX1相互作用的蛋白质——叶片倾斜度调控因子1（RLI1），它通过影响水稻叶枕细胞伸长来正向调控叶片倾斜度。rli1突变体叶片倾斜度降低，而RLI1过表达植株叶片倾斜度增加。RLI1直接激活下游基因油菜素内酯上调基因1（BU1）和类BU1复合体1来控制叶枕细胞的伸长，从而增强叶片倾斜度。我们还发现缺磷会抑制RLI1的表达。SPX1蛋白与RLI1直接相互作用，这可能会阻止RLI1与下游基因的启动子结合。因此，SPX和RLI1形成一个模块，以响应水稻外部磷的有效性来调控叶片倾斜度。