Plant mineral nutrition is critical for agricultural productivity and human nutrition. However, the availability of mineral elements is heterogeneous spatially and temporally in many ecosystems and agricultural landscapes. Nutrient imbalances trigger intricate signalling networks that modulate plant acclimation responses. One signalling agent of particular importance in such networks is melatonin, a pleiotropic molecule with multiple functions. Evidence indicates that nutrient deficiency or excess generally increases melatonin levels in particular tissues, and melatonin is increasingly thought to participate in the regulation of plant mineral nutrition. Alterations in endogenous melatonin levels could protect plants from oxidative stress, influence root architecture, and enhance the nutrient uptake and use efficiency through transcriptional and post-transcriptional regulation; such changes optimise mineral nutrient acquisition and ion homeostasis inside plant cells for plant growth promotion. This review summarises the current information on the regulation of plant mineral nutrition by melatonin and emphasises how endogenous melatonin alters plant responses to specific mineral elements. Furthermore, we comprehensively discuss how melatonin enhances nutrient uptake and transport under conditions of nutrient shortage.

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Lipid peroxidation is a common event during aluminum (Al) toxicity in plants, and it generates an array of aldehyde fragments. The present study investigated and compared the profile and physiological functions of lipid peroxide-derived aldehydes under Al stress in two wheat genotypes that differed in Al resistance. Under Al stress, the sensitive genotype Yangmai-5 suffered more severe plasma membrane damage and accumulated higher levels of aldehydes in roots than the Al-tolerant genotype Jian-864. The complementary use of high-resolution mass spectrometry and standard compounds allowed the identification and quantification of 13 kinds of short-chain aldehydes sourced from lipids in wheat roots. Among these aldehydes, acetaldehyde, isovaldehyde, valeraldehyde, (E)-2-hexenal (HE), heptaldehyde, and nonyl aldehyde were the predominant species. Moreover, it was found that HE in the sensitive genotype was over 2.63 times higher than that in the tolerant genotype after Al treatment. Elimination of aldehydes using carnosine rescued root growth inhibition by 19.59 and 11.63% in Jian-864 and Yangmai-5, respectively, and alleviated Al-induced membrane damage and protein oxidation. Exogenous aldehyde application further inhibited root elongation and exacerbated oxidative injury. The tolerant genotype Jian-864 showed elevated aldehyde detoxifying enzyme activity and transcript levels. These results suggest that lipid peroxide-derived short-chain aldehydes are involved in Al toxicity, and a higher aldehyde-detoxifying capacity may be responsible for Al tolerance.