Nitric Oxide Is Required for Melatonin-Enhanced Tolerance against Salinity Stress in Rapeseed (Brassica napus L.) Seedlings.
Nitric Oxide Is Required for Melatonin-Enhanced Tolerance against Salinity Stress in Rapeseed (Brassica napus L.) Seedlings.
复制标题
DOI：
10.3390/ijms19071912
复制
发表时间：
2018-06-29
影响因子：
5.6
通讯作者：
Shen W
中科院分区：
文献类型：
--
作者：
Zhao G;Zhao Y;Yu X;Kiprotich F;Han H;Guan R;Wang R;Shen W
褪黑激素（N-乙酰基-5-甲氧基色胺）虽然可以缓解植物的盐胁迫，但其下游的信号转导途径仍不完全清楚。在这里，我们报告，内源褪黑激素和此后的一氧化氮（NO）积累连续增加NaCl胁迫油菜（甘蓝型油菜L.）幼苗根褪黑激素和NO释放化合物的应用不仅抵消了NaCl诱导的幼苗生长抑制，但也重建氧化还原和离子稳态，其中后者证实了缓解活性氧的过度产生，硫代巴比妥酸反应物质的生产，和Na+/K+比的下降。因此，相关的抗氧化防御基因，钠氢交换器（NHX 1），和盐过度敏感2（SOS 2）转录调节。参与S-亚硝基化，氧化还原为基础的翻译后修饰触发NO，建议。进一步的结果表明，在响应NaCl胁迫，增加NO水平的增加，通过在幼苗根系中添加褪黑激素加强。上述反应可被NO清除剂清除NO所消除。我们进一步发现，NO的去除不改变内源性褪黑激素的含量在根中单独补充NaCl或与褪黑激素一起，从而排除NO触发褪黑激素生产的可能性。遗传学证据表明，与野生型拟南芥相比，在nia 1/2和noa 1突变体（表现出无效硝酸还原酶活性和间接降低内源NO水平，分别）不能拯救褪黑激素补充剂对NaCl的超敏反应。没有观察到氧化还原稳态的重建和SOS信号的诱导。总之，上述药理学、分子和遗传学数据得出结论，NO在褪黑激素下游起作用，促进盐耐受性。
Although melatonin (N-acetyl-5-methoxytryptamine) could alleviate salinity stress in plants, the downstream signaling pathway is still not fully characterized. Here, we report that endogenous melatonin and thereafter nitric oxide (NO) accumulation was successively increased in NaCl-stressed rapeseed (Brassica napus L.) seedling roots. Application of melatonin and NO-releasing compound not only counteracted NaCl-induced seedling growth inhibition, but also reestablished redox and ion homeostasis, the latter of which are confirmed by the alleviation of reactive oxygen species overproduction, the decreases in thiobarbituric acid reactive substances production, and Na+/K+ ratio. Consistently, the related antioxidant defense genes, sodium hydrogen exchanger (NHX1), and salt overly sensitive 2 (SOS2) transcripts are modulated. The involvement S-nitrosylation, a redox-based posttranslational modification triggered by NO, is suggested. Further results show that in response to NaCl stress, the increased NO levels are strengthened by the addition of melatonin in seedling roots. Above responses are abolished by the removal of NO by NO scavenger. We further discover that the removal of NO does not alter endogenous melatonin content in roots supplemented with NaCl alone or together with melatonin, thus excluding the possibility of NO-triggered melatonin production. Genetic evidence reveals that, compared with wild-type Arabidopsis, the hypersensitivity to NaCl in nia1/2 and noa1 mutants (exhibiting null nitrate reductase activity and indirectly reduced endogenous NO level, respectively) cannot be rescued by melatonin supplementation. The reestablishment of redox homeostasis and induction of SOS signaling are not observed. In summary, above pharmacological, molecular, and genetic data conclude that NO operates downstream of melatonin promoting salinity tolerance.
登录
查看更多内容
影响因子：
5.6
作者：
Corpas FJ;Alché JD;Barroso JB
通讯作者：
Barroso JB
影响因子：
10.3
作者：
Kang, Young-Soon;Kang, Yong-Gyu;Bae, Soo-Kyung
通讯作者：
Bae, Soo-Kyung
影响因子：
13.6
作者：
Chen, Meng;Cui, Weiti;Shen, Wenbiao
通讯作者：
Shen, Wenbiao
影响因子：
27.5
作者：
Han, Bin;Yang, Zheng;Shen, Wenbiao
通讯作者：
Shen, Wenbiao
影响因子：
10.3
作者：
COZZI, B;MOREI, G;REITER, RJ
通讯作者：
REITER, RJ