Scholarlink

<p><i>Ulva prolifera</i>, the primary causative species of green tide, has garnered significant attention due to its robust growth and reproductive capacity under high salt stress. However, there has been relatively little research on the regulation of high salt stress in this species. In this study, we observed that high salt stress suppressed the growth of <i>U. prolifera</i> and leading to the nitric oxide (NO) accumulation, along with increased gene expression levels and enzyme activity of S-nitrosoglutathione reductase (GSNOR). Treatment with GSNOR inhibitor resulted in elevated NO levels under high salt stress, accompanied by reduced activity of antioxidant enzymes and decreased glutathione (GSH) accumulation, making <i>U. prolifera</i> more sensitive to high salt stress. Conversely, NO scavenger treatment not only reduced NO levels, but also weakened the high salt stress tolerance of <i>U. prolifera</i>. Furthermore, using tandem mass tags (TMT) switch analysis and mass spectrometry, we observed a significant increase in S-nitrosylated protein levels in <i>U. prolifera</i> under high salt stress, with further augmentation upon GSNOR inhibitor treatment. We also found high salt stress induced S-nitrosylation (SNO) of glutathione reductase (GR), which is negatively regulated by GSNOR, resulting in increased GR activity. Our results show that under short-term high salt stress, the elevated expression level of GSNOR avoided excessive accumulation of NO, and a certain amount of NO enhanced the activity of antioxidant enzymes through SNO modification, which improve the high salt stress tolerance of <i>U. prolifera</i>, whereas under long-term high salt stress, excessive NO was toxic to <i>U. prolifera</i>.</p>

错误：搜索内容不能为空，请输入英文关键词
错误：关键词超出字数限制，请精简
高级检索

S-nitrosylation coordination enhances high salt tolerance in Ulva prolifera

  • 期刊论文

  • 发表日期：

    2025年4月25日

查看全文
  • Dongren Zhang,
  • Xiuwen Yang,
  • Jingwei Dong,
  • Hongyan He,
  • Aurang Zeb,
  • Ruyi Song,
  • Bing Han,
  • Songdong Shen

摘要

Ulva prolifera, the primary causative species of green tide, has garnered significant attention due to its robust growth and reproductive capacity under high salt stress. However, there has been relatively little research on the regulation of high salt stress in this species. In this study, we observed that high salt stress suppressed the growth of U. prolifera and leading to the nitric oxide (NO) accumulation, along with increased gene expression levels and enzyme activity of S-nitrosoglutathione reductase (GSNOR). Treatment with GSNOR inhibitor resulted in elevated NO levels under high salt stress, accompanied by reduced activity of antioxidant enzymes and decreased glutathione (GSH) accumulation, making U. prolifera more sensitive to high salt stress. Conversely, NO scavenger treatment not only reduced NO levels, but also weakened the high salt stress tolerance of U. prolifera. Furthermore, using tandem mass tags (TMT) switch analysis and mass spectrometry, we observed a significant increase in S-nitrosylated protein levels in U. prolifera under high salt stress, with further augmentation upon GSNOR inhibitor treatment. We also found high salt stress induced S-nitrosylation (SNO) of glutathione reductase (GR), which is negatively regulated by GSNOR, resulting in increased GR activity. Our results show that under short-term high salt stress, the elevated expression level of GSNOR avoided excessive accumulation of NO, and a certain amount of NO enhanced the activity of antioxidant enzymes through SNO modification, which improve the high salt stress tolerance of U. prolifera, whereas under long-term high salt stress, excessive NO was toxic to U. prolifera.