Nitrate reductase-dependent nitric oxide is crucial for multi-walled carbon nanotube-induced plant tolerance against salinity
文献类型: 外文期刊
作者: Zhao, Gan 1 ; Zhao, Yingying 1 ; Lou, Wang 1 ; Su, Jiuchang 1 ; Wei, Siqi 1 ; Yang, Xuemei 1 ; Wang, Ren 2 ; Guan, Rongzh 1 ;
作者机构: 1.Nanjing Agr Univ, Lab Ctr Life Sci, Coll Life Sci, Nanjing 210095, Jiangsu, Peoples R China
2.Jiangsu Prov & Chinese Acad Sci, Inst Bot, Nanjing 210014, Jiangsu, Peoples R China
3.Nanjing Agr Univ, State Key Lab Crop Genet & Germplasm Enhancement, Nanjing 210095, Jiangsu, Peoples R China
4.Jiangsu Acad Agr Sci, Inst Ind Crops, Jiangsu Collaborat Innovat Ctr Modern Crop Prod, Nanjing 210014, Jiangsu, Peoples R China
期刊名称:NANOSCALE ( 影响因子:7.79; 五年影响因子:7.632 )
ISSN: 2040-3364
年卷期: 2019 年 11 卷 21 期
页码:
收录情况: SCI
摘要: Although there have been some studies on the plant-carbonaceous nanomaterials (CNMs) interactions, related conclusions were controversial. Here, we report that multi-walled carbon nanotubes (MWCNTs) can enter into rapeseed (Brassica napus L.) seedling root, and transport to stem. Further results showed that salinity-inhibited rapeseed seedling growth was obviously alleviated by MWCNTs. Meanwhile, NaClinduced nitrate reductase (NR)-dependent NO production was significantly intensified by MWCNTs. The redox and ion imbalance was reestablished as well, confirmed by the reduction in reactive oxygen species (ROS) overproduction, the decrease in thiobarbituric acid reactive substance production, and the lower Na+/K+ ratio. These beneficial effects could be explained by the changes in related antioxidant defense genes, sodium hydrogen exchanger 1 (NHX1), salt overly sensitive 1 (SOS1), and K+ transporter 1 (KT1) transcripts. The above responses were separately abolished after the removal of endogenous NO with its scavengers or the addition of the NR inhibitor. Genetic evidence revealed that the NaCl-triggered NO level in wild-type seedling roots was partly abolished in either the nitric reductase mutant (nia1/2) or noa1 mutant (exhibiting indirectly a reduced endogenous NO level). Treatment with MWCNTs could totally rescue the impaired NO production in the noa1 mutant rather than the nia1/2 mutant, suggesting that NR-dependent NO acts as a downstream signaling molecule in MWCNT signaling. This point was verified by phenotypic analyses, histochemical staining, and ion analysis. qPCR analysis further demonstrated that MWCNTs stimulated antioxidant genes and ion balance-related genes through NR-mediated NO. The above molecular and genetic evidence indicated that NR-dependent NO acts downstream of MWCNTs in salinity tolerance, which requires the reestablishment of redox and ion homeostasis.
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