Ionic Liquid-Mediated Route to Atomic Layer Deposition of Tin(II) Oxide via a C-C Bond Cleavage Ligand Modification Mechanism.

Atomic layer deposition (ALD) is a technologically important method to grow thin films with high conformality and excellent thickness control from vapor phase precursors. The development of new thermal ALD processes can be limited by precursor reactivity and stability: reaction temperature and precursor design are among the few variables available to achieve higher reactivity in gas-phase reactions, unlike in solution synthesis, where the use of solvent and/or a catalyst can promote a desired reaction. To bridge this synthesis gap between vapor-phase and solution-phase, we demonstrate the use of an ultrathin coating layer of a vapor phase-compatible solvent─an ionic liquid (IL)─on our growth substrate to perform ALD of SnO. Successful SnO deposition is achieved using tin acetylacetonate and water, a process that otherwise would require a stronger counter-reactant such as ozone. The presence of the layer of IL allows a solvent-mediated reaction mechanism to take place on the growth substrate surface. We report a growth per cycle of 0.67 Å/cycle at a deposition temperature of 100 °C in an IL comprising 1-ethyl-3-methylimidazolium hydrogen sulfate. Characterization of the ALD films confirms the SnO film composition, and 1H and 13C NMR are used to probe the solvent-mediated ALD reaction, suggesting a solvent-mediated addition-elimination-type mechanism which breaks a C-C bond in acetylacetonate to form acetone and acetate. Density functional theory calculations show that the IL solvent is beneficial to the proposed solvent-mediated mechanism by lowering the C-C bond cleavage energetics of acetylacetonate compared to the vapor phase. A general class of ligand modification reactions for thermal ALD is thus introduced in this work.

Loss of Interleukin-13-Receptor-Alpha-1 Induces Apoptosis and Promotes EMT in Pancreatic Cancer.

In search of new therapies for pancreatic cancer, cytokine pathways have attracted increasing interest in recent years. Cytokines play a vital role in the crosstalk between tumour cells and the tumour microenvironment. The related inflammatory cytokines IL-4 and IL-13 can regularly be detected at increased levels in the microenvironment of pancreatic cancer. They share a receptor heterodimer consisting of IL-4Rα and IL-13Rα1. While IL-4Rα induces a more oncogenic phenotype, the role of IL-13Rα1 was yet to be determined. ShRNA-based knockdown of IL-13Rα1 was performed in Capan-1 and MIA PaCa-2. We assessed cell growth and migratory capacities under the influence of IL-13Rα1. Pathway alterations were detected by immunoblot analysis. We now have demonstrated that the loss of IL-13Rα1 induces apoptosis in pancreatic cancer cells. This was associated with an epithelial-to-mesenchymal transition. Loss of IL-13Rα1 also abolished the effects of exogenous IL-4 and IL-13 stimulation. Interestingly, in wild type cells, cytokine stimulation caused a similar increase in migratory capacities as after IL-13Rα1 knockdown. Overall, our results indicate the vital role of IL-13Rα1 in the progression of pancreatic cancer. The differential expression of IL-4Rα and IL-13Rα1 has to be taken into account when considering a cytokine-targeted therapy in pancreatic cancer.

Chemical Modifications of Ag Catalyst Surfaces with Imidazolium Ionomers Modulate H2 Evolution Rates during Electrochemical CO2 Reduction.

Bridging polymer design with catalyst surface science is a promising direction for tuning and optimizing electrochemical reactors that could impact long-term goals in energy and sustainability. Particularly, the interaction between inorganic catalyst surfaces and organic-based ionomers provides an avenue to both steer reaction selectivity and promote activity. Here, we studied the role of imidazolium-based ionomers for electrocatalytic CO2 reduction to CO (CO2R) on Ag surfaces and found that they produce no effect on CO2R activity yet strongly promote the competing hydrogen evolution reaction (HER). By examining the dependence of HER and CO2R rates on concentrations of CO2 and HCO3-, we developed a kinetic model that attributes HER promotion to intrinsic promotion of HCO3- reduction by imidazolium ionomers. We also show that varying the ionomer structure by changing substituents on the imidazolium ring modulates the HER promotion. This ionomer-structure dependence was analyzed via Taft steric parameters and density functional theory calculations, which suggest that steric bulk from functionalities on the imidazolium ring reduces access of the ionomer to both HCO3- and the Ag surface, thus limiting the promotional effect. Our results help develop design rules for ionomer-catalyst interactions in CO2R and motivate further work into precisely uncovering the interplay between primary and secondary coordination in determining electrocatalytic behavior.

Possible Roles of Interleukin-4 and -13 and Their Receptors in Gastric and Colon Cancer.

Interleukin (IL)-4 and -13 are structurally and functionally related cytokines sharing common receptor subunits. They regulate immune responses and, moreover, are involved in the pathogenesis of a variety of human neoplasms. Three different receptors have been described for IL-4, but only IL-4 receptor type II (IL-4Rα/IL-13Rα1) is expressed in solid tumors. While IL-13 can also bind to three different receptors, IL-13 receptor type I (IL-4Rα/IL-13Rα1/IL-13Rα2) and type II (IL-4Rα/IL-13Rα1) are expressed in solid tumors. After receptor binding, IL-4 and IL-13 can mediate tumor cell proliferation, survival, and metastasis in gastric or colon cancer. This review summarizes the results about the role of IL-4/IL-13 and their receptors in gastric and colon cancer.

Involvement of IL-4, IL-13 and Their Receptors in Pancreatic Cancer.

Interleukin (IL)-4 and IL-13 are known as pleiotropic Th2 cytokines with a wide range of biological properties and functions especially in immune responses. In addition, increasing activities have also been determined in oncogenesis and tumor progression of several malignancies. It is now generally accepted that IL-4 and IL-13 can exert effects on epithelial tumor cells through corresponding receptors. Type II IL-4 receptor (IL-4Rα/IL-13Rα1), predominantly expressed in non-hematopoietic cells, is identified to be the main target for both IL-4 and IL-13 in tumors. Moreover, IL-13 can also signal by binding to the IL-13Rα2 receptor. Structural similarity due to the use of the same receptor complex generated in response to IL-4/IL-13 results in overlapping but also distinct signaling pathways and functions. The aim of this review was to summarize knowledge about IL-4 and IL-13 and their receptors in pancreatic cancer in order understand the implication of IL-4 and IL-13 and their receptors for pancreatic tumorigenesis and progression and for developing possible new diagnostic and therapeutic targets.

The steps from sexual reproduction to apomixis.

MAIN CONCLUSION: In this paper, an interaction model of apomixis-related genes was constructed to analyze the emergence of apomictic types. It is speculated that apomixis technology will be first implemented in gramineous plants. Apomixis (asexual seed formation) is a phenomenon in which a plant bypasses the most fundamental aspects of sexual reproduction-meiosis and fertilization-to form a viable seed. Plants can form seeds without fertilization, and the seed genotype is consistent with the female parent. The development of apomictic technology would be revolutionary for agriculture and for food production as it would reduce costs and breeding times and also avoid many complications typical of sexual reproduction (e.g. incompatibility barriers) and of vegetative propagation (e.g. viral transfer). The application of apomictic reproductive technology has the potential to revolutionize crop breeding. This article reviews recent advances in apomixis in cytology and molecular biology. The general idea of identifying apomixis was proposed and the process of the emergence of non-fusion types was discussed. To better understand the apomixis mechanism, an apomixis regulatory model was established. At the same time, the realization of apomixis technology is proposed, which provides reference for the research and application of apomixis.

Astragaloside IV Protects Rat Cardiomyocytes from Hypoxia-Induced Injury by Down-Regulation of miR-23a and miR-92a.

BACKGROUND/AIMS: Astragaloside IV (AS-IV), a traditional Chinese medicine isolated from Astragalus membranaceus, has been shown to exert cardioprotective effect previously. This study aimed to reveal the effects of AS-IV on hypoxia-injured cardiomyocyte. METHODS: H9c2 cells were treated with various doses of AS-IV for 24 h upon hypoxia. CCK-8 assay, flow cytometry/Western blot, and qRT-PCR were respectively conducted to measure the changes in cell viability, apoptosis, and the expression of miR-23a and miR-92a. Sprague-Dawley rats were received coronary ligation, and were administrated by various doses of AS-IV for 14 days. The infarct volume and outcome of rats followed by ligation were tested by ultrasound, arteriopuncture and nitrotetrazolium blue chloride (NBT) staining. RESULTS: We found that 10 µg/ml of AS-IV exerted myocardioprotective effects against hypoxia-induced cell damage, as AS-IV significantly increased H9c2 cells viability and decreased apoptosis. Interestingly, the myocardioprotective effects of AS-IV were alleviated by miR-23a and/or miR-92a overexpression. Knockdown of miR-23a and miR-92a activated PI3K/AKT and MAPK/ ERK signaling pathways. Bcl-2 was a target gene for miR-23a, and BCL2L2 was a target gene for miR-92a. In the animal model of myocardial infarction (MI), AS-IV significantly reduced the infarct volume, ejection fraction (EF), shortening fraction (FS) and LV systolic pressure (LVSP), and significantly increased left ventricular end-diastolic internal diameter (LVEDd). And also, the elevated expression of miR-23a and miR-92a in MI rat was reduced by AS-IV. CONCLUSION: AS-IV protected cardiomyocytes against hypoxia-induced injury possibly via down-regulation of miR-23a and miR-92a, and via activation of PI3K/AKT and MAPK/ERK signaling pathways.

Patterns of Drought Response of 38 WRKY Transcription Factors of Zanthoxylum bungeanum Maxim.

The WRKY family of transcription factors (TFs) includes a number of transcription-specific groupings that play important roles in plant growth and development and in plant responses to various stresses. To screen for WRKY transcription factors associated with drought stress in Zanthoxylum bungeanum, a total of 38 ZbWRKY were identified and these were then classified and identified with Arabidopsis WRKY. Using bioinformatics analyses based on the structural characteristics of the conservative domain, 38 WRKY transcription factors were identified and categorized into three groups: Groups I, II, and III. Of these, Group II can be divided into four subgroups: subgroups IIb, IIc, IId, and IIe. No ZbWRKY members of subgroup IIa were found in the sequencing data. In addition, 38 ZbWRKY were identified by real-time PCR to determine the behavior of this family of genes under drought stress. Twelve ZbWRKY transcription factors were found to be significantly upregulated under drought stress and these were identified by relative quantification. As predicted by the STRING website, the results show that the WRKYs are involved in four signaling pathways-the jasmonic acid (JA), the salicylic acid (SA), the mitogen-activated protein kinase (MAPK), and the ethylene signaling pathways. ZbWRKY33 is the most intense transcription factor in response to drought stress. We predict that WRKY33 binds directly to the ethylene synthesis precursor gene ACS6, to promote ethylene synthesis. Ethylene then binds to the ethylene activator release signal to activate a series of downstream genes for cold stress and osmotic responses. The roles of ZbWRKY transcription factors in drought stress rely on a regulatory network center on the JA signaling pathway.

Long Non-Coding RNA H19 Protects H9c2 Cells against Hypoxia-Induced Injury by Targeting MicroRNA-139.

BACKGROUND/AIMS: Acute myocardial infarction (AMI) occurs when blood supply to the heart is diminished (ischemia) for long time; ischemia is primarily caused due to hypoxia. The present study evaluated the effects of long non-coding RNA H19 on hypoxic rat H9c2 cells and mouse HL-1 cells. METHODS: Hypoxic injury was confirmed by measuring cell viability, migration and invasion, and apoptosis using MTT, Transwell and flow cytometry assays, respectively. H19 expression after hypoxia was estimated by qRT-PCR. We then measured the effects of non-physiologically expressed H19, knockdown of miR-139 with or without H19 silence, and abnormally expressed Sox8 on hypoxia-induced H9c2 cells. Moreover, the interacted miRNA for H19 and downstream target gene were virtually screened and verified. The involved signaling pathways and the effects of abnormally expressed H19 on contractility of HL-1 cells were explored via Western blot analysis. RESULTS: Hypoxia induced decreases of cell viability, migration and invasion, increase of cell apoptosis and up-regulation of H19. Knockdown of H19 increased hypoxia-induced injury in H9c2 cells. H19 acted as a sponge for miR-139 and H19 knockdown aggravated hypoxia-induced injury by up-regulating miR-139. Sox8 was identified as a target of miR-139, and its expression was negatively regulated by miR-139. The mechanistic studies revealed that overexpression of Sox8 might decrease hypoxia-induced cell injury by activating the PI3K/AKT/mTOR pathway and MAPK. Besides, H19 promoted contractility of HL-1 cells. CONCLUSION: These findings suggest that H19 alleviates hypoxia-induced myocardial cell injury by miR-139-mediated up-regulation of Sox8, along with activation of the PI3K/AKT/mTOR pathway and MAPK.

ACTN4 and the pathways associated with cell motility and adhesion contribute to the process of lung cancer metastasis to the brain.

BACKGROUND: The aim of this study was to identify critical gene pathways that are associated with lung cancer metastasis to the brain. METHODS: The RNA-Seq approach was used to establish the expression profiles of a primary lung cancer, adjacent benign tissue, and metastatic brain tumor from a single patient. The expression profiles of these three types of tissues were compared to define differentially expressed genes, followed by serial-cluster analysis, gene ontology analysis, pathway analysis, and knowledge-driven network analysis. Reverse transcription-polymerase chain reaction (RT-PCR) was used to validate the expression of essential candidate genes in tissues from ten additional patients. RESULTS: Differential gene expression among these three types of tissues was classified into multiple clusters according to the patterns of their alterations. Further bioinformatic analysis of these expression profile data showed that the network of the signal transduction pathways related to actin cytoskeleton reorganization, cell migration, and adhesion was associated with lung cancer metastasis to the brain. The expression of ACTN4 (actinin, alpha 4), a cytoskeleton protein gene essential for cytoskeleton organization and cell motility, was significantly elevated in the metastatic brain tumor but not in the primary lung cancer tissue. CONCLUSIONS: The signaling pathways involved in the regulation of cytoskeleton reorganization, cell motility, and focal adhesion play a role in the process of lung cancer metastasis to the brain. The contribution of ACTN4 to the process of lung cancer metastasis to the brain could be mainly through regulation of actin cytoskeleton reorganization, cell motility, and focal adhesion.

Advancements in the diagnosis and treatment of sub­centimeter lung cancer in the era of precision medicine (Review).

Lung cancer is the malignancy with the highest global mortality rate and imposes a substantial burden on society. The increasing popularity of lung cancer screening has led to increasing number of patients being diagnosed with pulmonary nodules due to their potential for malignancy, causing considerable distress in the affected population. However, the diagnosis and treatment of sub-centimeter grade pulmonary nodules remain controversial. The evolution of genetic detection technology and the development of targeted drugs have positioned the diagnosis and treatment of lung cancer in the precision medicine era, leading to a marked improvement in the survival rate of patients with lung cancer. It has been established that lung cancer driver genes serve a key role in the development and progression of sub-centimeter lung cancer. The present review aimed to consolidate the findings on genes associated with sub-centimeter lung cancer, with the intent of serving as a reference for future studies and the personalized management of sub-centimeter lung cancer through genetic testing.

Identification of cytokines in benign and malignant thymus tumors: based on Mendelian randomization and proteomics.

Objective: The aim of this study was to identify potential causal cytokines in thymic malignancies and benign tumors from the FinnGen database using Mendelian randomization (MR). Methods: In this study, data from genome-wide association studies (GWAS) of 91 cytokines were used as exposure factors, and those of thymic malignant tumors and thymic benign tumors were the outcome variables. Two methods were used to determine the causal relationship between exposure factors and outcome variables: inverse variance weighting (IVW) and MR-Egger regression. Sensitivity analysis was performed using three methods, namely, the heterogeneity test, the pleiotropy test, and the leave-one-out test. Results: There was a causal relationship between the expression of fibroblast growth factor 5, which is a risk factor for thymic malignant tumors, and thymic malignant tumors. C-C motif chemokine 19 expression, T-cell surface glycoprotein CD5 levels, and interleukin-12 subunit beta levels were causally related to thymic malignant tumors and were protective. Adenosine deaminase levels, interleukin-10 receptor subunit beta expression, tumor necrosis factor (TNF)-related apoptosis-inducing ligand levels, and TNF-related activation-induced cytokine levels showed a causal relationship with thymic benign tumors, which are its risk factors. Caspase 8 levels, C-C motif chemokine 28 levels, interleukin-12 subunit beta levels, latency-associated peptide transforming growth factor beta 1 levels, and programmed cell death 1 ligand 1 expression showed a causal relationship with thymic benign tumors, which are protective factors. Sensitivity analysis showed no heterogeneity. Conclusion: Cytokines showed a causal relationship with benign and malignant thymic tumors. Interleukin-12 subunit beta is a common cytokine that affects malignant and benign thymic tumors.

Roles of IL-4, IL-13, and Their Receptors in Lung Cancer.

Interleukin (IL)-4 and IL-13 are the main effectors of innate lymphoid cells (ILC2) of the type 2 innate immune response, which can carry out specific signal transmission between multiple cells in the tumor immune microenvironment. IL-4 and IL-13 mediate signal transduction and regulate cellular functions in a variety of solid tumors through their shared receptor chain, the transmembrane heterodimer interleukin-4 receptor alpha/interleukin-13 receptor alpha-1 (type II IL-4 receptor). IL-4, IL-13, and their receptors can induce the formation of a variety of malignant tumors and play an important role in their progression, growth, and tumor immunity. In order to explore possible targets for lung cancer prediction and treatment, this review summarizes the characteristics and signal transduction pathways of IL-4 and IL-13, and their respective receptors, and discusses in depth their possible role in the occurrence and development of lung cancer.

High electrochemical active Au-NP/2D zinc-metal organic frameworks heterostructure-based ECL sensor for the miRNA-522 detection in triple negative breast cancer.

In this work, a novel electrochemiluminescence (ECL) sensor has been developed to detect the miRNA-522 in the tumor tissues of triple-negative breast cancer (TNBC) patients. Au NPs/Zn MOF heterostructure was obtained by in situ growth and used as novel luminescence probe. Firstly, zinc-metal organic framework nanosheets (Zn MOF NSs) were synthesized with Zn2+ as the central metal ion and 2-aminoterephthalic acid (NH2-BDC) as the ligand. 2D MOF nanosheets with ultra-thin layered structure and relatively large specific surface areas can enhance the catalytic activity in the ECL generation. Furthermore, the electron transfer capacity and the electrochemical active surface area of MOF were greatly improved by the growth of Au NPs. Therefore, Au NPs/Zn MOF heterostructure showed the significant electrochemical activity in the sensing process. In addition, the magnetic Fe3O4@SiO2@Au microspheres were used as capture units in the magnetic separation step. The magnetic spheres with hairpin aptamer H1 can capture target gene. Then the captured miRNA-522 triggered the target catalyzed hairpin assembly (CHA) sensing process and linked Au NPs/Zn MOF heterostructure. The concentration of miRNA-522 can be quantified by the ECL signal enhancement of the Au NPs/Zn MOF heterostructure. Due to the high catalytic activity of Au NPs/Zn MOF heterostructure and their unique structural and electrochemical properties, the prepared ECL sensor achieved high-sensitive detection of miRNA-522 in the range of 1 fM to 0.1 nM with the detection limit of 0.3 fM. This strategy can provide a potential alternative for miRNA detection in medical research and clinical diagnosis of triple negative breast cancer.

Evidence based on Mendelian randomization: Causal relationship between mitochondrial biological function and lung cancer and its subtypes.

OBJECTIVE: This study aimed to investigate the causal relationship between mitochondrial biological function and lung cancer, including its subtypes, via MR. METHODS: SNPs significantly associated with lung cancer and its subtypes were employed as instrumental variables. MR-Egger regression, simple mode, weighted mode, simple median, and weighted median, were utilized to determine the causal relationship between the exposure factor and the occurrence of lung cancer and its subtypes. RESULTS: NADH dehydrogenase (ubiquinone) flavoprotein 2 and transmembrane protein 70 were found to have a causal relationship with lung adenocarcinoma, acting as protective factors. The causal relationship between mitochondrial import inner membrane translocase subunit and NADH dehydrogenase (ubiquinone) iron-sulfur protein 4 and small-cell lung cancer was established as a risk factor. NADH dehydrogenase (ubiquinone) 1 beta subcomplex subunit 8 exhibited a causal relationship with small-cell lung cancer, acting as a protective factor. Furthermore, NAD-dependent protein deacylase sirtuin-5 was causally linked to lung squamous cell carcinoma, serving as a protective factor. A funnel plot demonstrated the symmetrical distribution of the SNPs. Thew pleiotroy test (P > 0.05) and "leave-one-out" test validated the relative stability of the results. CONCLUSION: This study established a causal relationship between mitochondrial biological function and lung cancer, including its subtypes.

Research progress of single-cell sequencing in tuberculosis.

Tuberculosis is a major infectious disease caused by Mycobacterium tuberculosis infection. The pathogenesis and immune mechanism of tuberculosis are not clear, and it is urgent to find new drugs, diagnosis, and treatment targets. A useful tool in the quest to reveal the enigmas related to Mycobacterium tuberculosis infection and disease is the single-cell sequencing technique. By clarifying cell heterogeneity, identifying pathogenic cell groups, and finding key gene targets, the map at the single cell level enables people to better understand the cell diversity of complex organisms and the immune state of hosts during infection. Here, we briefly reviewed the development of single-cell sequencing, and emphasized the different applications and limitations of various technologies. Single-cell sequencing has been widely used in the study of the pathogenesis and immune response of tuberculosis. We review these works summarizing the most influential findings. Combined with the multi-molecular level and multi-dimensional analysis, we aim to deeply understand the blank and potential future development of the research on Mycobacterium tuberculosis infection using single-cell sequencing technology.

ECL resonance energy transfer-regulated "off-on" mode biosensor for the detection of miRNA-150-5p in triple negative breast cancer.

MiRNAs played critical roles in triple negative breast cancer (TNBC) as potential biomarkers. Herein, an efficient signal "off-on" mode-biosensor based on electrochemiluminescence resonance energy transfer (ECL-RET) was successfully constructed for the miRNA-150-5p determination in TNBC. The ECL-RET regulated-sensing platform consisted of NiMn-LDHs nanoflowers, the artificially assembled phospholipid bilayers and hairpin DNA-labeled Eu-doped MoS2 QDs. Firstly, Eu-doped MoS2 QDs with high quantum efficiency were prepared as the ECL-RET donors. And NiMn-layer double hydroxides (LDHs) nanoflowers with wide UV-vis absorption spectra as the ECL-RET acceptors. Secondly, due to the hairpin DNA structure, the closed distance between ECL-RET donor-acceptor pair can quench the luminescence signal of Eu-doped MoS2 QDs. When miRNA-150-5p was captured, the hairpin DNA structure changed to a rodlike configuration and enlarged the distance between Eu-doped MoS2 QDs and NiMn-LDHs. As a result, the recovery of ECL signal can be observed as a signal "turn off-on" mode. Furthermore, the hydrophilicity of the lipid bilayer can reduce the nonspecific adsorption and improve the flexibility of the hairpin DNA efficiently. Therefore, based on the ECL-RET regulation strategy, the biosensor was employed to detect miRNA-150-5p from 10 fM to 1 nM with a detection limit of 1.5 fM. The constructed biosensor can effectively differentiate TNBC patient tumor and healthy breast fibroadenoma. The ECL-RET regulation strategy provided a new biosensing pathway for ultrasensitive detection of biomolecules and promoted the development of diagnosis and treatment of TNBC.

The role of post-transcriptional regulation in SARS-CoV-2 infection and pathogenicity.

The COVID-19 pandemic caused by the Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2) virus has had a significant impact on global social and economic stability. To combat this, researchers have turned to omics approaches, particularly epitranscriptomics, to limit infection and develop effective therapeutic strategies. Multi-omics can provide the host response dynamics during multiple disease phases to reveal the molecular and cellular landscapes. Epitranscriptomics focuses on the mechanisms of gene transcription in cells and tissues and the relationship between genetic material and epigenetic regulation. This review highlights the role of post-transcriptional regulation in SARS-CoV-2, which affect various processes such as virus infection, replication, immunogenicity, and pathogenicity. The review also explains the formation mechanism of post-transcriptional modifications and how they can be regulated to combat viral infection and pathogenicity.

Soil labile organic carbon fractions mediate microbial community assembly processes during long-term vegetation succession in a semiarid region.

Conceptual diagram for the labile organic carbon (OC) fractions mediating microbial assembly processes during long-term vegetation succession.

Molecular Cloning and Functional Analysis of DXS and FPS Genes from Zanthoxylum bungeanum Maxim.

Zanthoxylum bungeanum Maxim. (Z. bungeanum) has attracted attention for its rich aroma. The aroma of Z. bungeanum is mainly volatile terpenes synthesized by plant terpene metabolic pathways. However, there is little information on Z. bungeanum terpene metabolic gene. In this study, the coding sequence of 1-deoxy-D-xylulose-5-phosphate synthase (DXS) and farnesyl pyrophosphate synthase (FPS) were cloned from Z. bungeanum cv. 'Fengxiandahongpao.' ZbDXS and ZbFPS genes from Z. bungeanum with CDS lengths of 2172 bp and 1029 bp, respectively. The bioinformatics results showed that Z. bungeanum was closely related to citrus, and it was deduced that ZbFPS were hydrophilic proteins without the transmembrane domain. Subcellular localization prediction indicated that ZbDXS was most likely to be located in chloroplasts, and ZbFPS was most likely to be in mitochondria. Meanwhile, the 3D protein structure showed that ZbDXS and ZbFPS were mainly composed of α-helices, which were folded into a single domain. In vitro enzyme activity experiments showed that purified proteins ZbDXS and ZbFPS had the functions of DXS enzyme and FPS enzyme. Transient expression of ZbDXS and ZbFPS in tobacco significantly increased tobacco's terpene content. Moreover, ZbDXS and ZbFPS were expressed in different tissues of Z. bungeanum, and the relative expression of the two genes was the highest in fruits. Therefore, this suggests that ZbDXS and ZbFPS are positively related to terpene synthesis. This study could provide reference genes for improving Z. bungeanum breeding as well as for the Rutaceae research.