Nitric oxide participates in the regulation of LeCBF1 gene expression and improves cold tolerance in harvested tomato fruit

Nitric oxide (NO) is an important signal molecule involved in numerous plant responses to biotic and abiotic stress. C-repeat/dehydration-responsive element (CRT/DRE)-binding factors (CBFs) play a prominent role in cold response regulation. To investigate the relationship between NO and the CBF pathway during cold stress, tomato (Solanum lycopersicum cv. Lichun) fruit were treated with the NO donor (sodium nitroprusside, SNP) and nitric oxide synthase (NOS) inhibitor (N (omega)-nitro-l-arginine, l-NNA) before storage at 2 °C. Treatment with 0.02 mM SNP decreased the chilling injury (CI) index, whereas l-NNA treatment increased the appearance of chilling symptoms. NO content in fruit following SNP treatment was higher, while malondialdehyde (MDA) content and ion leakage were lower than that in water- and l-NNA-treated fruit. The relative expression of LeCBF1, measured by q-RTPCR, in SNP-treated fruit was higher than that in l-NNA-treated and control fruit after cold storage for 0.5 and 4 h. These results suggest that SNP treatment protects tomatoes from cold injury by inducing NO accumulation and expression of LeCBF1. NOS activity may play a role in NO accumulation associated with cold tolerance.

► Postharvest chilling injury in tomato fruit is reduced by raising fruit nitrous oxide (NO) content with sodium nitroprusside.
► The NO synthase (NOS) inhibitor (l-NNA) inhibited NO content and increased fruit chilling injury.
► The NOS pathway is important for postharvest NO synthesis in tomato fruit with respect to low temperature tolerance.
► Cold tolerance is associated with LeCBF1 gene expression.