One of the important goals of crop breeding is yield improvement. Among the yield indices, the tiller angle is tightly associated with enhancing photosynthetic efficiency and facilitating enhanced planting density (Sakamoto et al., 2006; Wang and Li, 2008). Rice plants with erect tillers, leaves and panicles allow a high‐density planting system for high yields but are more susceptible to the occurrence of sheath blight disease causing yield reduction. Therefore, the antagonistic relationship between crop yield and immunity pathways makes crop breeding extremely difficult (Ning et al., 2017). In our previous studies, we found that overexpression of loose plant architecture 1 (LPA1) reduced the tiller and lamina joint angle but increased resistance to sheath blight disease through activation of PIN1a‐mediated auxin distribution, suggesting the breeding potential of LPA1 in high‐density planting systems (Liu et al., 2016; Sun et al., 2019). To further analyse the mechanism of tiller angle and sheath blight regulation, we performed a yeast two‐hybrid selection and identified G‐protein γ subunit DEP1 (dense and erect panicle 1, Os09g26999) as a novel interactor of LPA1. The heterotrimeric G proteins, comprising α, β and γ subunits, are key players in the transmission of extracellular signals via membrane‐spanning G‐protein‐coupled receptors to intracellular effectors (Gilman, 1987), and panicle erectness is controlled by a dominant allele of DEP1, which reduces the length of the inflorescence internode (Huang et al., 2009). Further analysis indicated that DEP1 interacted with both full‐length LPA1 and its N‐terminal region (indeterminate domain, IDD) (Figure 1a). Furthermore, coimmunoprecipitation (co‐IP) and split‐GFP assays confirmed that LPA1 interacted with DEP1 in the nucleus (Figure 1b,c)
紋枯病是中國水稻三大病害之一，是目前發(fā)病面積和防治面積最大的一個病害。但在生產(chǎn)中抗紋枯病的水稻品種較少，抗病機制研究還有待深入。前期研究中發(fā)現(xiàn)，轉(zhuǎn)錄因子IDD14/LPA1通過轉(zhuǎn)錄激活生長素極性運輸?shù)鞍譖IN1a正調(diào)控水稻分蘗角度和對紋枯病的抗性。酵母雙雜交、BiFC和免疫共沉淀實驗結(jié)果證實，G‐protein γ subunit DEP1與LPA1的N段（IDD結(jié)構(gòu)域）互作。dep1突變體相比野生型對照Dongjin（韓國栽培稻）分蘗角小，且抗紋枯病。遺傳學實驗結(jié)果證實，dep1/lpa1分蘗和抗病表型與lpa1突變體類似，揭示LPA1在DEP1下游調(diào)節(jié)水稻分蘗角和對紋枯病的抗性，但具體調(diào)控機制不清楚。
進一步研究結(jié)果證實，DEP1突變不影響LPA1蛋白水平，但DEP1抑制LPA1結(jié)合PIN1a啟動子的活性，揭示DEP1可能通過抑制LPA1轉(zhuǎn)錄激活下游基因PIN1a，從而調(diào)控水稻分蘗角和對紋枯病的抗性。