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Abscisic acid–inducible NAC32 alleviates magnesium toxicity-mediated cell death in roots through direct regulation of XIPOTL1 expression in Arabidopsis.

Cadmium (Cd) pollution seriously reduces the yield and quality of vegetables. Reducing Cd accumulation in vegetables is of great significance for improving food safety and sustainable agricultural development. Here, using tomato as the material, we analyzed the effect of foliar spraying with zinc oxide nanoparticles (ZnO NPs) on Cd accumulation and tolerance in tomato seedlings. Foliar spraying with ZnO NPs improved Cd tolerance by increasing photosynthesis efficiency and antioxidative capacity, while it reduced Cd accumulation by 40.2% in roots and 34.5% in leaves but increased Zn content by 33.9% in roots and 78.6% in leaves. Foliar spraying with ZnO NPs also increased the contents of copper (Cu) and manganese (Mn) in the leaves of Cd-treated tomato seedlings. Subsequent metabonomic analysis showed that ZnO NPs exposure alleviated the fluctuation of metabolic profiling in response to Cd toxicity, and it had a more prominent effect in leaves than in roots. Correlation analysis revealed that several differentially accumulated metabolites were positively or negatively correlated with the growth parameters and physiol-biochemical indexes. We also found that flavonoids and alkaloid metabolites may play an important role in ZnO NP-alleviated Cd toxicity in tomato seedlings. Taken together, the results of this study indicated that foliar spraying with ZnO NPs effectively reduced Cd accumulation in tomato seedlings; moreover, it also reduced oxidative damage, improved the absorption of trace elements, and reduced the metabolic fluctuation caused by Cd toxicity, thus alleviating Cd-induced growth inhibition in tomato seedlings. This study will enable us to better understand how ZnO NPs regulate plant growth and development and provide new insights into the use of ZnO NPs for improving growth and reducing Cd accumulation in vegetables.

As one of the components of root exudates, methyl 3-(4-hydroxyphenyl) propionate (MHPP) not only functions as a nitrification inhibitor in soil but also modulates plant growth and root system architecture (RSA); however, the physiological and molecular mechanisms underlying MHPP-mediated plant growth remain largely unclear. Here, we investigated the effects of MHPP treatment on growth and secondary metabolite accumulation by integrating physiology, transcriptome and metabolome analyses using perilla (Perilla frutescens), a type of medicinal and edible plant. MHPP reduces primary root growth but markedly induces lateral root formation in perilla seedlings. The full-length transcript sequencing combined with the comparative transcriptomic analysis revealed that the differential expression of genes involved in carbon/nitrogen metabolism and secondary metabolism contributed to the MHPP-mediated plant growth. An investigation of the differentially expressed genes showed that MHPP modulates the growth and metabolism of leaves and roots in distinct pathways. The genes involved in the phenylpropanoid metabolism pathway showed opposite expression patterns between the roots and leaves, thereby resulting in the differential accumulation of secondary metabolites in the roots and leaves. Furthermore, the differential expression of PER genes and elevated peroxidase activity in the MHPP-treated roots were responsible for modulating the equilibrium of ROS and the components of lignin and phenolic compounds, thereby affecting plant growth and secondary metabolite accumulation. MHPP modulates RSA and metabolite profiles and improves the contents of medicinal ingredients in perilla plants. These results suggested that the application of MHPP may represent a useful strategy for the medicinal plant cultivation.

Abscisic acid (ABA) reduces accumulation of potentially toxic cadmium (Cd) in plants. How the ABA signal is transmitted to modulate Cd uptake remains largely unclear. Here, we report that the basic region/Leu zipper transcription factor ABSCISIC ACID-INSENSITIVE5 (ABI5), a central ABA signaling molecule, is involved in ABA-repressed Cd accumulation in plants by physically interacting with a previously uncharacterized R2R3-type MYB transcription factor, MYB49. Overexpression of the Cd-induced MYB49 gene in Arabidopsis (Arabidopsis thaliana) resulted in a significant increase in Cd accumulation, whereas myb49 knockout plants and plants expressing chimeric repressors of MYB49:ERF-associated amphiphilic repression motif repression domain (SRDX49) exhibited reduced accumulation of Cd. Further investigations revealed that MYB49 positively regulates the expression of the basic helix-loop-helix transcription factors bHLH38 and bHLH101 by directly binding to their promoters, leading to activation of IRON-REGULATED TRANSPORTER1, which encodes a metal transporter involved in Cd uptake. MYB49 also binds to the promoter regions of the heavy metal-associated isoprenylated plant proteins (HIPP22) and HIPP44, resulting in up-regulation of their expression and subsequent Cd accumulation. On the other hand, as a feedback mechanism to control Cd uptake and accumulation in plant cells, Cd-induced ABA up-regulates the expression of ABI5, whose protein product interacts with MYB49 and prevents its binding to the promoters of downstream genes, thereby reducing Cd accumulation. Our results provide new insights into the molecular feedback mechanisms underlying ABA signaling-controlled Cd uptake and accumulation in plants.

Studies have indicated that the carbon starvation response leads to the reprogramming of the transcriptome and metabolome, and many genes, including several important regulators, such as the group S1 basic leucine zipper transcription factors (TFs) bZIP1, bZIP11 and bZIP53, the SNAC-A TF ATAF1, etc., are involved in these physiological processes. Here, we show that the SNAC-A TF ANAC032 also plays important roles in this process. The overexpression of ANAC032 inhibits photosynthesis and induces reactive oxygen species accumulation in chloroplasts, thereby reducing sugar accumulation and resulting in carbon starvation. ANAC032 reprograms carbon and nitrogen metabolism by increasing sugar and amino acid catabolism in plants. The ChIP-qPCR and transient dual-luciferase reporter assays indicated that ANAC032 regulates trehalose metabolism via the direct regulation of TRE1 expression. Taken together, these results show that ANAC032 is an important regulator of the carbon/energy status that represses photosynthesis to induce carbon starvation.

Background Melatonin and serotonin are well-known signaling molecules that mediate multiple physiological activities in plants, including stress defense, growth, development, and morphogenesis, but their underlying mechanisms have not yet been thoroughly elucidated. In this study, we investigated the roles of melatonin and serotonin in modulating plant growth and defense by integrating physiological and transcriptome analyses in Arabidopsis. Results Moderate concentrations of melatonin and serotonin did not affect primary root (PR) growth but markedly induced lateral root (LR) formation. Both melatonin and serotonin locally induced the expression of the cell-wall-remodeling-related genes LBD16 and XTR6, thereby inducing LR development. Our data support the idea that melatonin and serotonin lack any auxin-like activity. Treatment with 50 μM serotonin significantly improved PSII activity, and the transcriptome data supported this result. Melatonin and serotonin slightly affected glycolysis and the TCA cycle; however, they markedly regulated the catabolism of several key amino acids, thereby affecting carbon metabolism and energy metabolism. Melatonin and serotonin improved iron (Fe) deficiency tolerance by inducing Fe-responsive gene expression. Conclusions Overall, our results from the physiological and transcriptome analyses reveal the roles of melatonin and serotonin in modulating plant growth and stress responses and provide insight into novel crop production strategies using these two phytoneurotransmitters. Electronic supplementary material The online version of this article (10.1186/s12870-018-1548-2) contains supplementary material, which is available to authorized users.