Mutation of G-protein γ subunit DEP1 increases planting density and resistance to sheath blight disease in rice.
Mutation of G-protein γ subunit DEP1 increases planting density and resistance to sheath blight disease in rice.
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G蛋白γ亚基DEP1突变提高水稻种植密度和对纹枯病的抗性
DOI：
10.1111/pbi.13500
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发表时间：
2021-03
影响因子：
13.8
通讯作者：
Hu Xuan Y
中科院分区：
文献类型：
--
作者：
Miao Liu J;Mei Q;Yun Xue C;Yuan Wang Z;Pin Li D;Xin Zhang Y;Hu Xuan Y
作物育种的重要目标之一是提高产量。在产量指标中，分蘖角度与提高光合作用效率和促进种植密度密切相关(Sakamoto等人，2006；Wang和Li，2008)。具有直立的分蘖、叶片和圆锥花序的水稻植株为高产提供了高密度种植系统，但更容易发生纹枯病，导致减产。因此，作物产量和免疫途径之间的对立关系使作物育种极其困难(Ning等人，2017)。在我们之前的研究中，我们发现过表达松散植物架构1(LPA1)通过激活PIN1a介导的生长素分配而减少了分蘖和叶片关节角度，但提高了对纹枯病的抗性，这表明LPA1在高密度种植系统中具有育种潜力(Liu等人，2016；Sun等人，2019)。为了进一步分析分蘖角度和纹枯病的调控机制，我们进行了酵母双杂交选择，确定G蛋白c亚基DEP1(密集直立的穗状花序1，Os09g26999)是LPA1的一个新的互作因子。由a、b和c亚基组成的异三聚体G蛋白是通过跨膜G蛋白偶联受体向细胞内效应器传递细胞外信号的关键角色(Gilman，1987)，而穗的直立受DEP1的显性等位基因控制，DEP1减少了花序节间的长度(Huang等人，2009年)。进一步的分析表明，DEP1既与全长LPA1相互作用，又与其N-末端区域(不确定结构域，IDD)相互作用(图1a)。此外，免疫共沉淀(co-IP)和Split-GFP分析证实LPA1与DEP1在细胞核内相互作用(图1b，c)。通过qPCR，我们发现DEP1在叶鞘中的表达高于在叶、根和花中的表达(图1D)。接种立枯丝核菌诱导了LPA1，但不诱导DEP1(图1e)，DEP1-GFP定位于质膜和细胞核(图1f)。为了分析DEP1在水稻品种东锦中的功能，以DEP1RNAi系为材料，构建了DEP1基因敲除突变体DEP1-Ko(An et al.，2003)(Pfg_3A-02648)。Northern杂交结果表明，DEP1在两个RNAi系(#1和#3)中的表达被抑制了约50%，而在DEP1-Ko中没有检测到它的表达
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 c subunit DEP1 (dense and erect panicle 1, Os09g26999) as a novel interactor of LPA1. The heterotrimeric G proteins, comprising a, b and c 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). Through qPCR, we found that DEP1 expression in sheaths is high compared with that in leaves, roots and flowers (Figure 1d). Rhizoctonia solani inoculation induced LPA1, but not DEP1 (Figure 1e), and DEP1-GFP was localized at the plasma membrane and nucleus (Figure 1f). To analyse DEP1 function in the japonica rice cultivar Dongjin, a DEP1 knockout mutant dep1-ko (An et al., 2003)(PFG_3A-02648) with the T-DNA inserted into the first intron, and DEP1 RNAi lines were used. Northern blot results confirmed that DEP1 expression was suppressed by about 50% in two RNAi lines (# 1 and# 3) while it was not detected in dep1-ko
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影响因子：
14.9
作者：
Kozaki, A;Hake, S;Colasanti, J
通讯作者：
Colasanti, J
影响因子：
7.4
作者：
An, SY;Park, S;An, GH
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松散植物结构1，一种参与芽向地性的不确定域蛋白，调节水稻的植物结构
影响因子：
7.4
作者：
Wu, Xinru;Tang, Ding;Cheng, Zhukuan
通讯作者：
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影响因子：
6.9
作者：
Liu JM;Park SJ;Huang J;Lee EJ;Xuan YH;Je BI;Kumar V;Priatama RA;Raj K V;Kim SH;Min MK;Cho JH;Kim TH;Chandran AK;Jung KH;Takatsuto S;Fujioka S;Han CD
通讯作者：
Han CD
影响因子：
46.9
作者：
Sakamoto, T;Morinaka, Y;Matsuoka, M
通讯作者：
Matsuoka, M