The function of inositol 1,4,5-trisphosphate (IP3) in nitric oxide (NO)-induced chilling tolerance in postharvest kiwifruit was revealed. The fruit were treated using sodium nitroprusside (SNP; exogenous NO donor) and neomycin (IP3 inhibitor). Data demonstrated that compared with the control, chilling injury (CI) index and firmness decreased and increased upon SNP treatment in kiwifruit. SNP treatment enhanced phosphoinositide-specific phospholipase C (PI-PLC) activity, and consequently induced IP3 production. Moreover, SNP treatment down regulated malondialdehyde (MDA) content and electrolyte leakage as well as the activity and gene expression of lipoxygenase (LOX) in kiwifruit. In addition, the gene expression of transcription factors, including C-repeat binding factor1 (CBF1), WRKY1 and NAC5 was induced by SNP treatment. The above effects induced upon SNP treatment were inhibited by neomycin treatment. Neomycin treatment alone also led to the increase in CI index, MDA content and electrolyte leakage as well as the activity and gene expression of LOX, and the decrease in firmness, PI-PLC activity and IP3 production and gene expression of CBF1, WRKY1 and NAC5. Thus, IP3 mediated the alleviation of membrane damage, and the induction of CBF1, WRKY1 and NAC5 by SNP, thereby delaying CI in kiwifruit.

揭示了肌醇1,4,5-三磷酸酯（IP3）在一氧化氮（NO）诱导的猕猴桃耐寒性中的作用。使用硝普钠（SNP；外源NO供体）和新霉素（IP3抑制剂）处理果实。数据表明，与对照组相比，猕猴桃经SNP处理后冷害（CI）指数和硬度均降低和升高。SNP处理提高了磷酸肌醇特异性磷脂酶C（PI-PLC）的活性，并因此诱导了IP3的产生。此外，SNP处理降低了猕猴桃中丙二醛（MDA）含量和电解质渗漏以及脂氧合酶（LOX）的活性和基因表达。另外，通过SNP处理诱导了转录因子的基因表达，包括C-重复结合因子1，CRK1和NAC5。新霉素治疗抑制了SNP治疗诱导的上述作用。单独使用新霉素也可导致CI指数，MDA含量和电解质渗漏以及LOX的活性和基因表达增加，而硬度，PI-PLC活性和IP3产量和基因表达下降。CBF1，WRKY1和NAC5。因此，IP3介导了膜损伤的减轻，以及SNP对CBF1，WRKY1和NAC5的诱导，从而延迟了奇异果中的CI。