The role of glycogen synthase kinase-3 (GSK-3) in nitric oxide (NO)-enhanced chilling tolerance in postharvest peach fruit was investigated. The fruits were immersed in sodium nitroprusside (SNP; exogenous NO donor) and bikinin (GSK-3 inhibitor). Results showed that the chilling injury (CI) index declined following the exposure of the peach fruit to exogenous SNP. SNP treatment also induced GSK-3 expression. Furthermore, SNP treatment reduced malondialdehyde (MDA) content and electrolyte leakage in the peach fruit. In addition, SNP treatment induced the increase in alternative oxidase (AOX) activity and the upregulation of the gene expression of 18.1-kDa class I heat shock protein (HSP), WRKY2, and C-repeat binding factor (CBF). The effects of SNP treatment were partly weakened by the addition of bikinin. These findings indicate that GSK-3 mediated the reduction of MDA content and electrolyte leakage and the activation of AOX, 18.1-kDa class I HSP, WRKY2, and CBF by NO, thereby inducing chilling tolerance in peach fruit.

研究了糖原合酶激酶3（GSK-3）在桃果实采后一氧化氮（NO）增强耐寒性中的作用。将果实浸入硝普钠（SNP；外源NO供体）和比基尼（GSK-3抑制剂）中。结果表明，将桃果实暴露于外源SNP后，冷害指数下降。SNP治疗也诱导了GSK-3表达。此外，SNP处理可降低桃果实中的丙二醛（MDA）含量和电解质泄漏。此外，SNP处理诱导了替代氧化酶（AOX）活性的增加和18.1kDa I类热休克蛋白（HSP），WRKY2和C重复结合因子（CBF）的基因表达上调。SNP处理的效果由于添加了比基尼而部分减弱。这些发现表明，GSK-3通过NO介导了MDA含量和电解质泄漏的减少以及AOX，18.1kDa I类HSP，WRKY2和CBF的活化，从而诱导了桃果实的耐冷性。