Root–shoot communication has a critical role in plant adaptation to environmental stress. Grafting is widely applied to enhance the abiotic stress tolerance of many horticultural crop species; however, the signal transduction mechanism involved in this tolerance remains unknown. Here, we show that pumpkin- or figleaf gourd rootstock-enhanced cold tolerance of watermelon shoots is accompanied by increases in the accumulation of melatonin, methyl jasmonate (MeJA), and hydrogen peroxide (H2O2). Increased melatonin levels in leaves were associated with both increased melatonin in rootstocks and MeJA-induced melatonin biosynthesis in leaves of plants under cold stress. Exogenous melatonin increased the accumulation of MeJA and H2O2 and enhanced cold tolerance, while inhibition of melatonin accumulation attenuated rootstock-induced MeJA and H2O2 accumulation and cold tolerance. MeJA application induced H2O2 accumulation and cold tolerance, but inhibition of JA biosynthesis abolished rootstock- or melatonin-induced H2O2 accumulation and cold tolerance. Additionally, inhibition of H2O2 production attenuated MeJA-induced tolerance to cold stress. Taken together, our results suggest that melatonin is involved in grafting-induced cold tolerance by inducing the accumulation of MeJA and H2O2. MeJA subsequently increases melatonin accumulation, forming a self-amplifying feedback loop that leads to increased H2O2 accumulation and cold tolerance. This study reveals a novel regulatory mechanism of rootstock-induced cold tolerance.
As one of the most destructive pests, aphids cause significant damage on various agricultural and horticultural crops. Recently, melatonin has been shown to enhance plant resistance to aphids; however, the underlying mechanisms remain unclear. In this study, our results showed that melatonin, MeJA, and H2S enhanced aphid resistance of watermelon in a dose‐dependent manner, accompanied by increases in the defense‐related enzyme activities and lignin accumulation. On the plants pretreated with 100 μM melatonin, 100 μM MeJA, and 50 μM NaHS, the numbers of aphids were 86.0%, 59.6%, and 47.9% lower than that on control plants, respectively, after aphid infestation for 7 days. Melatonin application induced MeJA and H2S accumulation in response to aphid infestation, while inhibition of MeJA and H2S accumulation attenuated or abolished melatonin‐induced defense response and aphid resistance, suggestive of the involvement of MeJA and H2S in melatonin‐induced aphid resistance. MeJA also increased H2S accumulation, but inhibition of MeJA biosynthesis prevented melatonin‐enhanced H2S accumulation, suggesting that MeJA mediates melatonin‐induced H2S accumulation. Furthermore, inhibition of H2S production attenuated MeJA‐induced defense response and aphid resistance. Taken together, the current study reveals a novel mechanism in which MeJA‐dependent H2S signaling is involved in melatonin‐induced defense response and subsequent aphid resistance. The increasing concern to minimize the use of pesticides and to switch onto sustainable and natural control strategies indicates the great exploitation of such a mechanism in combating aphids.
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