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Premature leaf senescence 3, encoding a methyltransferase, is required for melatonin biosynthesis in rice
The Plant Journal ( IF 6.2 ) Pub Date : 2018-07-19 , DOI: 10.1111/tpj.13995
Yongbo Hong 1, 2 , Yingxin Zhang 1, 2 , Sittipun Sinumporn 1, 2 , Ning Yu 1, 2 , Xiaodeng Zhan 1, 2 , Xihong Shen 1, 2 , Daibo Chen 1, 2 , Ping Yu 1, 2 , Weixun Wu 1, 2 , Qunen Liu 1, 2 , Zhaoyun Cao 3 , Chunde Zhao 1, 2 , Shihua Cheng 1, 2 , Liyong Cao 1, 2
Affiliation  

Premature leaf senescence in rice is one of the most common factors affecting the plant's development and yield. Although methyltransferases are involved in diverse biological functions, their roles in rice leaf senescence have not been previously reported. In this study, we identified the premature leaf senescence 3 (pls3) mutant in rice, which led to early leaf senescence and early heading date. Further investigations revealed that premature leaf senescence was triggered by the accumulation of reactive oxygen species. Using physiological analysis, we found that chlorophyll content was reduced in the pls3 mutant leaves, while hydrogen peroxide (H2O2) and malondialdehyde levels were elevated. Consistent with these findings, the pls3 mutant exhibited hypersensitivity to exogenous hydrogen peroxide. The expression of other senescence‐associated genes such as Osh36 and RCCR1 was increased in the pls3 mutant. Positional cloning indicated the pls3 phenotype was the result of a mutation in OsMTS1, which encodes an O‐methyltransferase in the melatonin biosynthetic pathway. Functional complementation of OsMTS1 in pls3 completely restored the wild‐type phenotype. We found leaf melatonin content to be dramatically reduced in pls3, and that exogenous application of melatonin recovered the pls3 mutant's leaf senescence phenotype to levels comparable to that of wild‐type rice. Moreover, overexpression of OsMTS1 in the wild‐type plant increased the grain yield by 15.9%. Our results demonstrate that disruption of OsMTS1, which codes for a methyltransferase, can trigger leaf senescence as a result of decreased melatonin production.

中文翻译:

水稻中褪黑激素生物合成需要编码甲基转移酶的过早叶片衰老3

水稻叶片早衰是影响植物发育和产量的最常见因素之一。尽管甲基转移酶参与多种生物学功能,但它们在水稻叶片衰老中的作用尚未见报道。在这项研究中,我们确定了水稻中的早叶衰老3pls3)突变体,从而导致了早叶衰老和抽穗期的提前。进一步的研究表明,叶片过早衰老是由活性氧的积累引起的。使用生理学分析,我们发现pls3突变体叶片中的叶绿素含量降低,而过氧化氢(H 2 O 2)和丙二醛水平升高。与这些发现一致,pls3突变体表现出对外源过氧化氢的超敏性。在pls3突变体中,其他与衰老相关的基因如Osh36RCCR1的表达增加。定位克隆指示的PLS3表型是在一个突变的结果OsMTS1,其编码在所述褪黑激素的生物合成途径的O-甲基转移酶。在pls3OsMTS1的功能互补完全恢复了野生型表型。我们发现在pls3中叶片褪黑激素含量显着降低,褪黑激素的外源应用使pls3突变体的叶片衰老表型恢复到与野生型水稻相当的水平。此外,野生型植物中OsMTS1的过度表达使谷物产量增加了15.9%。我们的结果表明,OsMTS1(编码甲基转移酶)的破坏可由于褪黑激素生成减少而触发叶片衰老。
更新日期:2018-07-19
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