Nitric oxide (NO) and nitrosylated derivatives are produced in peroxisomes, but the impact of NO metabolism on organelle functions remains largely uncharacterised. Double and triple NO‐related mutants expressing cyan florescent protein (CFP)‐SKL (nox1 × px‐ck and nia1 nia2 × px‐ck) were generated to determine whether NO regulates peroxisomal dynamics in response to cadmium (Cd) stress using confocal microscopy. Peroxule production was compromised in the nia1 nia2 mutants, which had lower NO levels than the wild‐type plants. These findings show that NO is produced early in the response to Cd stress and was involved in peroxule production. Cd‐induced peroxisomal proliferation was analysed using electron microscopy and by the accumulation of the peroxisomal marker PEX14. Peroxisomal proliferation was inhibited in the nia1 nia2 mutants. However, the phenotype was recovered by exogenous NO treatment. The number of peroxisomes and oxidative metabolism were changed in the NO‐related mutant cells. Furthermore, the pattern of oxidative modification and S‐nitrosylation of the catalase (CAT) protein was changed in the NO‐related mutants in both the absence and presence of Cd stress. Peroxisome‐dependent signalling was also affected in the NO‐related mutants. Taken together, these results show that NO metabolism plays an important role in peroxisome functions and signalling.

中文翻译：

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一氧化氮对于镉诱导的过氧化物的形成和过氧化物酶体的增殖是必不可少的。

过氧化物酶体中产生一氧化氮（NO）和亚硝酰化衍生物，但NO代谢对细胞器功能的影响仍未完全阐明。使用共聚焦显微镜产生了表达蓝绿色荧光蛋白（CFP）-SKL（nox1 × px-ck和nia1 nia2 × px-ck）的双和三态NO相关突变体，以确定NO是否调节过氧化物酶体动力学，使用共聚焦显微镜。Peroxule产量受到损害NiAl的nia2突变体，其NO水平低于野生型植物。这些发现表明NO在对Cd胁迫的响应中早期产生并且参与过氧化物的产生。使用电子显微镜和过氧化物酶体标记物PEX14的积累来分析Cd诱导的过氧化物酶体增殖。过氧化物酶体增殖在nia1 nia2突变体中受到抑制。然而，通过外源NO处理恢复了表型。NO相关突变细胞中过氧化物酶体的数量和氧化代谢发生了变化。此外，氧化修饰和S的模式无论是否存在镉胁迫，NO相关突变体中过氧化氢酶（CAT）蛋白的亚硝基化都发生了变化。过氧化物酶体依赖性信号在NO相关突变体中也受到影响。综上，这些结果表明，NO代谢在过氧化物酶体功能和信号传导中起着重要作用。