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• W4304080367 abstract "Excessive nitrogen (N) supply often leads to an imbalance of carbon (C) and N metabolism and inhibits plant growth. Sucrose, an important source and signaling substance of C in plants, is closely linked to N metabolism. However, it is not clear whether exogenous sucrose can mitigate the inhibitory effect of high N on plant growth by regulating C and N metabolism. In this study, we investigated the effects of exogenous sucrose on the growth, N metabolism, and C assimilation in the apple rootstock M26 seedlings under normal (5 mM NO3－, NN) and high (30 mM NO3－, HN) NO3－ concentrations. Our results showed that high NO3－ supply reduced plant growth, photosynthesis, and chlorophyll fluorescence, but spraying with 1% sucrose (HN + 1% Sucrose) significantly alleviated this inhibition. Application of 1% sucrose increased sucrose and sorbitol contents as well as sucrose-phosphate synthase and sucrose synthase activities in the plants under HN treatment and promoted the distribution of 13C photoassimilation products to the root. In addition, spraying with 1% sucrose alleviated the inhibition of N metabolizing enzyme activities by high NO3－ supply, reduced NO3－ accumulation and N content, increased free amino acid content, and promoted 15N distribution to the aboveground parts. However, spraying with 1% sucrose under the NN treatment negatively affected plant photosynthesis and carbon assimilation. In conclusion, exogenous sucrose increased the C level in plants in the presence of excess N, promoted the balance of C and N metabolism, and alleviated the inhibitory effect of high N on the apple plant growth." @default.
• W4304080367 created "2022-10-10" @default.
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• W4304080367 date "2022-12-01" @default.
• W4304080367 modified "2023-09-27" @default.
• W4304080367 title "Exogenous sucrose promotes the growth of apple rootstocks under high nitrate supply by modulating carbon and nitrogen metabolism" @default.
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• W4304080367 doi "https://doi.org/10.1016/j.plaphy.2022.10.005" @default.
• W4304080367 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/36244192" @default.
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