Increased anthropogenic activities over the last decades have led to a gradual increase in cadmium content in the soil, which, due to its high mobility in soil, makes Cd accumulation in plants a serious threat to the health of animals and humans. Plant hormones including melatonin (Mel) and brassinosteroids (BR) are known to provide tolerance against various abiotic stresses. In this work, the role of combined and separate exogenous application of Mel and BR on Cd stress in cherry tomato plants was examined. Cd stress significantly reduced tomato growth by inducing oxidative stress and reduced K+ uptake in roots and shoots. Combined application of Mel and BR reduced detrimental effects of Cd in tomato by (i) reducing Cd accumulation in the shoot; (ii) increasing the activities of different antioxidants (SOD, CAT, APX, GR); (iii) triggering higher expression of genes relating to Cd vacuolar sequestration (Na+/H+ EXCHANGER, SlNHX1; NATURAL RESISTANCE-ASSOCIATED MACROPHAGE PROTEIN 6, SlNRAMP6), and Cd transport and detoxification (HEAVY-METAL-ASSOCIATED 3, SlHMA3; PLANT CADMIUM RESISTANT 2, SlPCR2); and (iv) improving plant K+ homeostasis and contents in root and shoot. The latter trait was associated with the reduced gene expression of K+-permeable outward rectifying channel (SlGORK3), and transcriptional upregulation of high affinity potassium transporter 5 (SIHAK5) under Cd stress. A separate application of Mel and BR showed tissue-specific regulation of tomato growth and Cd tolerance by regulating antioxidant activities, K+ uptake, Cd uptake, and translocation from root to shoot and their endogenous contents. Melatonin per se was more effective in improving Cd tolerance in shoot while beneficial BR effects were more pronounced in roots, and their combined application was effective in both tissues. Taken together, reported results show tissue-specific regulation of Cd tolerance by Mel and BR in cherry tomato plants and demonstrate the efficiency of combined Mel + BR treatment as a practical tool to reduce Cd accumulation and mitigate its negative effects on plant growth.

Cadmium (Cd) exerts a toxic influence on numerous crucial growth and development processes in plants, notably affecting seed germination rate, transpiration rate, chlorophyll content, and biomass. While considerable advances in Cd uptake and detoxification of plants have been made, the mechanisms by which plants adapt to and tolerate Cd toxicity remain elusive. This review focuses on the relationship between Cd and plants and the prospects for phytoremediation of Cd pollution. We highlight the following issues: (1) the present state of Cd pollution and its associated hazards, encompassing the sources and distribution of Cd and the risks posed to human health; (2) the mechanisms underlying the uptake and transport of Cd, including the physiological processes associated with the uptake, translocation, and detoxification of Cd, as well as the pertinent gene families implicated in these processes; (3) the detrimental effects of Cd on plants and the mechanisms of detoxification, such as the activation of resistance genes, root chelation, vacuolar compartmentalization, the activation of antioxidant systems and the generation of non-enzymatic antioxidants; (4) the practical application of phytoremediation and the impact of incorporating exogenous substances on the Cd tolerance of plants.

Endoplasmic reticulum-associated degradation (ERAD) plays a critical role in the destruction of terminally misfolded proteins at the secretory pathway. The system also regulates expression levels of several proteins such as Pca1p, a cadmium exporter in yeast. To gain better insight into the mechanisms underlying ERAD of Pca1p and other polytopic proteins by the proteasome in the cytosol, our study determined the roles for the molecular factors of ERAD in dislodging Pca1p from the endoplasmic reticulum (ER). Inactivation of the 20S proteasome leads to accumulation of ubiquitinated Pca1p in the ER membrane, suggesting a role for the proteasome in extraction of Pca1p from the ER. Pca1p formed a complex with the proteasome at the membrane in a Doa10p E3 ligase-dependent manner. Cdc48p is required for recruiting the proteasome to Pca1p. Although the Ufd2p E4 ubiquitin chain extension enzyme is involved in efficient degradation of Pca1p, Ufd2p-deficient cells did not affect the formation of a complex between Pca1p and the proteasome. Two other polytopic membrane proteins undergoing ERAD, Ste6*p and Hmg2p, also displayed the same outcomes observed for Pca1p. However, poly-ubiquitinated Cpy1*p, a luminal ERAD substrate, was detected in the cytosol independent of proteolytic activities of the proteasome. These results indicate that extraction and degradation of polytopic membrane proteins at the ER is a coupled event. This mechanism would relieve the cost of exposed hydrophobic domains in the cytosol during ERAD.

Serine/arginine-rich (SR) proteins are important splicing factors. However, the biological functions of plant SR proteins remain unclear especially in abiotic stresses. Cadmium (Cd) is a non-essential element that negatively affects plant growth and development. In this study, we provided clear evidence for SR gene involved in Cd tolerance in planta. Systemic expression analysis of 17 Arabidopsis SR genes revealed that SR34b is the only SR gene upregulated by Cd, suggesting its potential roles in Arabidopsis Cd tolerance. Consistent with this, a SR34b T-DNA insertion mutant (sr34b) was moderately sensitive to Cd, which had higher Cd(2+) uptake rate and accumulated Cd in greater amounts than wild-type. This was due to the altered expression of iron-regulated transporter 1 (IRT1) gene in sr34b mutant. Under normal growth conditions, IRT1 mRNAs highly accumulated in sr34b mutant, which was a result of increased stability of IRT1 mRNA. Under Cd stress, however, sr34b mutant plants had a splicing defect in IRT1 gene, thus reducing the IRT1 mRNA accumulation. Despite of this, sr34b mutant plants still constitutively expressed IRT1 proteins under Cd stress, thereby resulting in Cd stress-sensitive phenotype. We therefore propose the essential roles of SR34b in posttranscriptional regulation of IRT1 expression and identify it as a regulator of Arabidopsis Cd tolerance.