The Systemic Acquired Resistance Regulator OsNPR1 Attenuates Growth by Repressing Auxin Signaling through Promoting IAA-Amido Synthase Expression
The Systemic Acquired Resistance Regulator OsNPR1 Attenuates Growth by Repressing Auxin Signaling through Promoting IAA-Amido Synthase Expression
复制标题
系统获得性抗性调节剂 OsNPR1 通过促进 IAA-酰胺合酶表达来抑制生长素信号传导，从而减弱生长。
DOI：
10.1104/pp.16.00129
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发表时间：
2016-09-01
期刊：
影响因子：
7.4
通讯作者：
He, Zuhua
中科院分区：
文献类型：
--
作者：
Li, Xiaozun;Yang, Dong-Lei;He, Zuhua
系统获得性抗性是一种持久、广谱的对病原菌的抗性。我们前期的研究表明，水稻病程相关基因NONEXPRESSOR(OsNPR1)的过表达大大提高了水稻对水稻白叶枯病的抗性，该基因是水稻系统获得抗性的主要基因。然而，OsNPR1过表达(OsNPR1-ox)植株的生长发育受到抑制，其机制尚不清楚。在本研究中，我们剖析了OsNPR1诱导的生长抑制。我们发现，OsNPR1-OX品系表现出与生长素缺失突变体相似的表型，表现在根系、种子数量和重量、节间伸长和分蘖数量减少。全基因组表达分析表明，与生长素代谢和信号通路相关的基因在OsNPR1-OX和野生型植物中存在差异表达。在OsNPR1-OX植株中，吲哚-3-乙酸(IAA)的含量一直在下降，生长素的分布格局也发生了变化。重要的是，我们发现一些GH3家族成员，特别是编码IAA-氨基合成酶的OsGH3.8，在OsNPR1-OX植物中结构性上调。通过RNA干扰降低OsGH3.8的表达可以部分恢复IAA水平，并在很大程度上挽救受抑制的生长发育表型，但不影响OsNPR1-OX植株的抗病能力。综上所述，我们揭示了OsNPR1至少部分通过间接上调OsGH3.8的表达来影响生长素途径，从而影响水稻的生长发育。
Systemic acquired resistance is a long-lasting and broad-spectrum disease resistance to pathogens. Our previous study demonstrated that overexpression of NONEXPRESSOR OF PATHOGENESIS-RELATED GENES1 (OsNPR1), a master gene for systemic acquired resistance in rice (Oryza sativa), greatly enhanced resistance to bacterial blight caused by Xanthomonas oryzae pv oryzae. However, the growth and development of the OsNPR1 overexpression (OsNPR1-OX) plants were restrained, and the mechanism remained elusive. In this study, we dissected the OsNPR1-induced growth inhibition. We found that the OsNPR1-OX lines displayed phenotypes mimicking auxin-defective mutants, with decreases in root system, seed number and weight, internode elongation, and tiller number. Whole-genome expression analysis revealed that genes related to the auxin metabolism and signaling pathway were differentially expressed between the OsNPR1-OX and wild-type plants. Consistently, the indole-3-acetic acid (IAA) content was decreased and the auxin distribution pattern was altered in OsNPR1-OX plants. Importantly, we found that some GH3 family members, in particular OsGH3.8 coding IAA-amido synthetase, were constitutively up-regulated in OsNPR1-OX plants. Decreased OsGH3.8 expression by RNA interference could partially restore IAA level and largely rescue the restrained growth and development phenotypes but did not affect the disease resistance of OsNPR1-OX plants. Taken together, we revealed that OsNPR1 affects rice growth and development by disrupting the auxin pathway at least partially through indirectly up-regulating OsGH3.8 expression.