Nitric oxide (NO) is a widely distributed gaseous signaling molecule in plants that can be synthesized through enzymatic and non-enzymatic pathways and plays an important role in plant growth and development, signal transduction, and response to biotic and abiotic stresses. Cadmium (Cd) is a heavy metal pollutant widely found in the environment, which not only inhibits plant growth but also enters humans through the food chain and endangers human health. To reduce or avoid the adverse effects of Cd stress, plants have evolved a range of coping mechanisms. Many studies have shown that NO is also involved in the plant response to Cd stress and plays an important role in regulating the resistance of plants to Cd stress. However, until now, the mechanisms by which Cd stress regulates the level of endogenous NO accumulation in plant cells remained unclear, and the role of exogenous NO in plant responses to Cd stress is controversial. This review describes the pathways of NO production in plants, the changes in endogenous NO levels in plants under Cd stress, and the effects of exogenous NO on regulating plant resistance to Cd stress.

SUMMARY Modification of the O‐acetylation level of xyloglucan (XyG) appears to affect aluminum (Al) sensitivity in Arabidopsis by modulating its binding capacity to Al. However, the transcriptional regulation of this process remains largely unknown. In our previous studies, we found that the expression of TRICHOME BIREFRINGENCE‐LIKE27 (TBL27), which is responsible for the O‐acetylation of XyG, was downregulated under Al stress. In the present study, we showed that the expression of an R2R3‐type transcription factor‐encoding gene, MYB103, was also inhibited by Al exposure and exhibited a co‐expression pattern with TBL27 in roots and siliques, suggesting a potential link between MYB103 and TBL27. The loss of function of MYB103 resulted in increased Al sensitivity, as indicated by more inhibited root growth and elevated root Al content compared with the wild type. Moreover, we also detected increased Al accumulation in the root cell wall and the hemicellulose fraction, which was attributed to the changes in the O‐acetylation level of XyG rather than the XyG content itself. In addition, further analysis revealed that MYB103 positively activated TBL27 expression by directly binding to the TBL27 promoter region, and TBL27 overexpression in the myb103 mutant rescued the Al‐sensitive phenotype of the mutant to the wild‐type level. Taken together, we conclude that MYB103 acts upstream of TBL27 to positively regulate Al resistance by modulating the O‐acetylation of the cell wall XyG.