Metal tolerance proteins (MTPs) as Me²⁺/H⁺(K⁺) antiporters participate in the transport of divalent cations, leading to heavy metal stress resistance and mineral utilization in plants. In the present study, to obtain better knowledge of the biological functions of the MTPs family, 20 potential EgMTPs genes were identified in Eucalyptus grandis and classified into seven groups belonging to three cation diffusion facilitator groups (Mn-CDFs, Zn/Fe-CDFs, and Zn-CDFs) and seven groups. EgMTP-encoded amino acids ranged from 315 to 884, and most of them contained 4–6 recognized transmembrane domains and were clearly prognosticated to localize into the cell vacuole. Almost all EgMTP genes experienced gene duplication events, in which some might be uniformly distributed in the genome. The numbers of cation efflux and the zinc transporter dimerization domain were highest in EgMTP proteins. The promoter regions of EgMTP genes have different cis-regulatory elements, indicating that the transcription rate of EgMTP genes can be a controlled response to different stimuli in multiple pathways. Our findings provide accurate perception on the role of the predicted miRNAs and the presence of SSR marker in the Eucalyptus genome and clarify their functions in metal tolerance regulation and marker-assisted selection, respectively. Gene expression profiling based on previous RNA-seq data indicates a probable function for EgMTP genes during development and responses to biotic stress. Additionally, the upregulation of EgMTP6, EgMTP5, and EgMTP11.1 to excess Cd²⁺ and Cu²⁺ exposure might be responsible for metal translocation from roots to leaves.

Methyl chavicol and methyl eugenol are important phenylpropanoid compounds previously purified from basil. These compounds are significantly enhanced by the water deficit stress-dependent mechanism. Here, for the first time, pObCVOMT and pObEOMT promoters were extracted by the genome walking method. They were then cloned into the upstream of the β-glucuronidase (GUS) reporter gene to identify the pattern of GUS water deficit stress-specific expression. Histochemical GUS assays showed in transgenic tobacco lines bearing the GUS gene driven by pObCVOMT and pObEOMT promoters, GUS was strongly expressed under water deficit stress. qRT-PCR analysis of pObCVOMT and pObEOMT transgenic plants confirmed the histochemical assays, indicating that the GUS expression is also significantly induced and up-regulated by increasing density of water deficit stress. This shows these promoters can drive inducible expression. The cis-acting elements analysis showed that the pObCVOMT and pObEOMT promoters contained dehydration or water deficit-related transcriptional control elements.

Background. Still, cancer remains to be one of the main causes of death globally. Sesquiterpene lactones (SLs) appeared to have remarkable pharmacologic properties, particularly as anticancer. This study evaluated the cytotoxicity and apoptogenic potential of Janerin and its underlying mechanism in HL60, THP‐1, and Jurkat leukemia cell lines vs. normal peripheral blood mononuclear cells (PBMCs). Methods. The viability of leukemia and PBMCs following treatment with Janerin (2.5–20 μM) and doxorubicin (2 μM, as the positive control) for 48 h was determined via the resazurin assay. The apoptotic cells were determined by annexin V and propidium iodide test. Also, the genes expressions involved in apoptosis were detected by real‐time PCR. Results. Janerin reduced cell viability in leukemia cells in a dose‐dependent manner with no significant toxicity toward normal PBM cells. Janerin significantly increased apoptosis in leukemia cells after 48 h of treatment. In these cells, the expressions of p21, p53, CASP3, CASP9, and Bax/Bcl2 ratio were significantly elevated, whereas CASP8 remained unchanged (p < 0.01). It was suggested that the intrinsic pathway was the mechanism by which Janerin induced apoptosis in HL60, THP‐1, and Jurkat leukemia cells in a time‐ and dose‐dependent manner. Conclusion. The findings imply that Janerin might be a suitable substitute for doxorubicin in leukemia patients.