Abscisic acid and putrescine synergistically regulate the cold tolerance of melon seedlings

Low temperature in early spring severely endangers the growth and development of melon seedlings. Abscisic acid (ABA) and polyamines (PAs) are important signal molecules in plant response to stress. However, the issue of whether they interact to regulate melon cold tolerance remains largely uncharacterized. Here, we identified a total of 14 key genes related to ABA and PAs biosynthesis, including four CmNCEDs, and ten genes in PA pathway (one CmADC, one CmODC, four CmSAMDCs, two CmSPDSs, and two CmSPAMs). Two oriental melon cultivars (IVF571, cold-tolerant; IVF004, cold-sensitive) were selected to explore the difference of ABA and PAs biosynthesis under cold stress (15 degrees C/6 degrees C, day/night). Results showed that the expressions of CmNCED3, CmNCED3-2, CmADC, CmSAMDCs, CmSPDS2 and CmSPMS1 were significantly up-regulated. ABA and putrescine levels were significantly increased in IVF571 under cold stress. Inhibiting the biosynthesis of endogenous ABA with nordihydroguaiaretic acid (NDGA) or Put with D-Arginine (D-Arg) dramatically decreased the levels of each other and aggravated the cold injury of melon seedlings. In addition, spraying with exogenous 75 mu M ABA or 1 mM Put improved the activities of superoxide dismutase, catalase and ascorbate peroxidase, and reduced the membrane lipid peroxidation damage of melon seedlings under cold stress. In all, the higher cold tolerance of IVF571 seedlings than that of IVF004 seedlings might be related to the increase in ABA and Put levels triggered by cold stress. ABA and Put could regulate the biosynthesis of each other and might act as signals to trigger the antioxidant system, thereby increasing melon cold tolerance.

Automated summary

The study found that under cold stress, the levels of ABA and putrescine in melon seedlings increase, enhancing cold tolerance. ABA and putrescine may regulate each other's synthesis, triggering the antioxidant system and reducing membrane lipid peroxidation damage.