Transcriptome analysis of flower colour reveals the correlation between SNP and differential expression genes in Phalaenopsis

Ding Yu,Wang Ma-Yin,Yang Ding-Hai,Hao Dai-Cheng,Li Wei-Shi,Ling Peng,Xie Shang-Qian 한국유전학회 2023 Genes & Genomics Vol.45 No.12

Background Phalaenopsis is an important ornamental plant that has great economic value in the world flower market as one of the most popular flower resources. Objective To investigate the flower colour formation of Phalaenopsis at the transcription level, the genes involved in flower color formation were identified from RNA-seq in this study. Methods In this study, white and purple petals of Phalaenopsis were collected and analyzed to obtained (1) differential expression genes (DEGs) between white and purple flower color and (2) the association between single nucleotide polymorphisms (SNP) mutations and DEGs at the transcriptome level. Results The results indicated that a total of 1,175 DEGs were identified, and 718 and 457 of them were up- and down-regulated genes, respectively. Gene Ontology and pathway enrichment showed that the biosynthesis of the secondary metabolites pathway was key to color formation, and the expression of 12 crucial genes (C4H, CCoAOMT, F3’H, UA3’5’GT, PAL, 4CL, CCR, CAD, CALDH, bglx, SGTase, and E1.11.17) that are involved in the regulation of flower color in Phalaenopsis. Conclusion This study reported the association between the SNP mutations and DEGs for color formation at RNA level, and provides a new insight to further investigate the gene expression and its relationship with genetic variants from RNA-seq data in other species.

Kernel Reference Set and Its Computation Algorithm

Ding-Yuan Bian,Qi-Wei Ge,Qian Zhu,Qian-Ming Shao 대한전자공학회 2008 ITC-CSCC :International Technical Conference on Ci Vol.2008 No.7

This paper proposes a new concept of graphs: kernel reference set. A kernel reference set is a fraction of vertices in a graph such that if their positions are known, positions of all other vertices can be derived from information of the distance matrix. We present an algorithm to find kernel reference set of graphs. Because the problem of kernel reference set is firstly proposed in this paper, and the theoretical limit of computation complexity is unknown currently. So we implement our algorithm with C to do the simulation. From simulation results, we verified the validity of our algorithm and evaluate its performance. Inspired by anchor nodes in wireless sensor networks, kernel reference set could be used to analyze anchorbased localization schemes of WSNs applications such as coalmine security monitoring, etc.

Relationship among porcine lncRNA TCONS_00010987, miR-323, and leptin receptor based on dual luciferase reporter gene assays and expression patterns

Ding, Yueyun,Qian, Li,Wang, Li,Wu, Chaodong,Li, DengTao,Zhang, Xiaodong,Yin, Zongjun,Wang, Yuanlang,Zhang, Wei,Wu, Xudong,Ding, Jian,Yang, Min,Zhang, Liang,Shang, Jinnan,Wang, Chonglong,Gao, Yafei Asian Australasian Association of Animal Productio 2020 Animal Bioscience Vol.33 No.2

Objective: Considering the physiological and clinical importance of leptin receptor (LEPR) in regulating obesity and the fact that porcine LEPR expression is not known to be controlled by lncRNAs and miRNAs, we aim to characterize this gene as a potential target of SSC-miR-323 and the lncRNA TCONS_00010987. Methods: Bioinformatics analyses revealed that lncRNA TCONS_00010987 and LEPR have SSC-miR-323-binding sites and that LEPR might be a target of lncRNA TCONS_00010987 based on cis prediction. Wild-type and mutant TCONS_00010987-target sequence fragments and wild-type and mutant LEPR 3'-UTR fragments were generated and cloned into pmiRRB-REPORT^TM-Control vectors to construct respective recombinant plasmids. HEK293T cells were co-transfected with the SSC-miR-323 mimics or a negative control with constructs harboring the corresponding binding sites and relative luciferase activities were determined. Tissue expression patterns of lncRNA TCONS_00010987, SSC-miR-323, and LEPR in Anqing six-end-white (AQ, the obese breed) and Large White (LW, the lean breed) pigs were detected by real-time quantitative polymerase chain reaction; backfat expression of LEPR protein was detected by western blotting. Results: Target gene fragments were successfully cloned, and the four recombinant vectors were constructed. Compared to the negative control, SSC-miR-323 mimics significantly inhibited luciferase activity from the wild-type TCONS_00010987-target sequence and wild-type LEPR-3'-UTR (p<0.01 for both) but not from the mutant TCONS_00010987-target sequence and mutant LEPR-3'-UTR (p>0.05 for both). Backfat expression levels of TCONS_00010987 and LEPR in AQ pigs were significantly higher than those in LW pigs (p<0.01), whereas levels of SSC-miR-323 in AQ pigs were significantly lower than those in LW pigs (p<0.05). LEPR protein levels in the backfat tissues of AQ pigs were markedly higher than those in LW pigs (p<0.01). Conclusion: LEPR is a potential target of SSC-miR-323, and TCONS_00010987 might act as a sponge for SSC-miR-323 to regulate LEPR expression.

Ethanol enhances cucurbitacin B-induced apoptosis by inhibiting cucurbitacin B-induced autophagy in LO2 hepatocytes

Qian Ding,Jiaolin Bao,Wenwen Zhao,Jinjian Lu,Hong Zhu,Xiuping Chen,Xiuping Chen 대한독성 유전단백체 학회 2016 Molecular & cellular toxicology Vol.12 No.1

Ethanol is a common risk factor for liver injury. Cucurbitacin B (CuB) is a natural product with potent cytotoxic activities mediated by inducing apoptosis. This study investigated the effect of ethanol on CuB-induced cytotoxicity in LO2 hepatocytes. Low concentration of ethanol alone showed no significant cytotoxic effect on LO2 cells. CuB dose-dependently decreased cell viability. However, ethanol co-treatment significantly enhanced CuB-induced cytotoxicity. CuB-induced mitochondria membrane potential (ΔΨ) depolarization was further decreased by ethanol. Furthermore, CuB-induced apoptosis was augmented by ethanol, as evidenced by DNA fragmentation, Annexin V staining, and apoptotic protein expression. Ethanol inhibited CuB-induced autophagy, as determined by MDC staining, autophagic protein expression, and transmission electron microscopy. Therefore, the present data suggested that ethanol enhanced CuB cytotoxicity in LO2 hepatocytes, which was mediated by inhibiting autophagy and augmenting apoptosis.

Site Preference of Alloying Elements in DO22-Ni3V Phase: Phase-Field and First-Principles Study

Ding-Ni Zhang,Qian-Qian Shangguan,Fu Liu,Ming-Yi Zhang 대한금속·재료학회 2015 METALS AND MATERIALS International Vol.21 No.4

Site preference of alloying elements in DO22-Ni3V phase was investigated using phase-field and first-principles method. The concentrations of alloying elements on sublattices of DO22-Ni3V phase were quantitatively studied using phase-field model based on microscopic diffusion equations. The phase-field computation results demonstrate that the concentration differences of alloying elements on the NiI and NiII site are attributed to the coordination environment difference. Host atoms Ni and substitutional ternary additions Al prefer to occupy NiI site. Antisite atoms V show site preference on the NiII site. Further reason of site preference of alloying elements on the two different Ni sites were studied using first-principles method to calculate the electronic structure of DO22-Ni3V phase. Calculation of density of states, orbitals population and charge population of the optimized Ni3V structure found that the electronic structures of NiI and NiII sites are different. Electronic structure difference, which is caused by coordination environment difference, is the essential reason for site selectivity behaviors of alloying elements on NiI and NiII sites.

The role of the apoptosis-related protein BCL-B in the regulation of mitophagy in hepatic stellate cells during the regression of liver fibrosis

Qian Ding,Xiao-Li Xie,Miao-Miao Wang,Jie Yin,Jin-Mei Tian,Xiao-Yu Jiang,Di Zhang,Jing Han,Yun Bai,Zi-Jin Cui,Hui-Qing Jiang 생화학분자생물학회 2019 Experimental and molecular medicine Vol.51 No.-

The clearance of activated hepatic stellate cells (HSCs) by apoptosis is critical for the reversibility of hepatic fibrosis. Mitochondrial homeostasis is regulated by mitophagy, which is an efficient way of clearing injured mitochondria that plays an important role in apoptosis. However, the role of mitophagy in apoptosis in HSCs and hepatic fibrosis is still unclear. Here, we show that mitophagy is enhanced in parallel with increased apoptosis in hepatic stellate cells during the reversal of hepatic fibrosis. The inhibition of mitophagy suppressed apoptosis in HSCs and aggravated hepatic fibrosis in mice. In contrast, the activation of mitophagy induced apoptosis in HSCs. Furthermore, we confirmed that BCL-B, which is a member of the BCL-2 family, is a regulator mediating mitophagy-related apoptosis. The knockdown of BCL-B resulted in increased apoptosis and mitophagy in HSCs, while the overexpression of BCL-B caused the opposite effects. BCL-B inhibited the phosphorylation of Parkin (a key regulator of mitophagy) and directly bound phospho-Parkin. Altogether, enhanced mitophagy promotes apoptosis in HSCs during the reversal of hepatic fibrosis. BCL-B suppresses mitophagy in HSCs by binding and suppressing phospho-Parkin, thereby inhibiting apoptosis. BCLB- dependent mitophagy is a new pathway for the regulation of apoptosis in HSCs during the regression of hepatic fibrosis

Preparation and Characterization of Acid and Pepsin-soluble Collagens from Scales of Croceine and Redlip Croakers

Qian-Qian Wu,Tao Li,Bin Wang,Guo-Fang Ding 한국식품과학회 2015 Food Science and Biotechnology Vol.24 No.6

Acid-soluble (ASC) and pepsin-soluble collagen (PSC) from scales of croceine croaker (ASCPC and PSC-PC) and redlip croaker (ASC-PP and PSC-PP) were prepared with yields of 0.37±0.08% (ASCPC), 1.09±0.23% (PSC-PC), 0.42±0.09% (ASC-PP), and 1.14±0.30% (PSC-PP) (dry scale basis). Gly (347.1- 359.8 residues/1,000 residues) was the major amino acid. Contents of imino acid were between 189.4 and 192.9 residues/1,000 residues in all 4 collagens. ASC-PC and ASC-PP were type I collagens. Differences in subunit components between ASC and PSC were observed. Denaturation temperature values of ASC-PC, ASC-PP, PSC-PC, and PSC-PP were 30.7, 30.1, 27.5, and 26.6℃, respectively. All 4 collagens were soluble at pH 1-4. Values declined when NaCl concentrations exceeded 2%. Freeze-dried collagens showed loose, fibrous, and porous structures. The 4 scale collagens can be alternatives to collagen from terrestrial animals for applications in functional food, cosmetic, and biomedical industries.

Relationship between porcine miR-20a and its putative target low-density lipoprotein receptor based on dual luciferase reporter gene assays

Yueyun Ding,Shujiao Zhu,Chaodong Wu,Li Qian,DengTao Li,Li Wang,Yuanlang Wang,Wei Zhang,Min Yang,Jian Ding,Xudong Wu,Xiao-Dong Zhang,Yafei Gao,Zongjun Yin 아세아·태평양축산학회 2019 Animal Bioscience Vol.32 No.7

Objective: Mutations in low-density lipoprotein receptor (LDLR), which encodes a critical protein for cholesterol homeostasis and lipid metabolism in mammals, are involved in cardiometabolic diseases, such as familial hypercholesterolemia in pigs. Whereas microRNAs (miRNAs) can control LDLR regulation, their involvement in circulating cholesterol and lipid levels with respect to cardiometabolic diseases in pigs is unclear. We aimed to identify and analyze LDLR as a potential target gene of SSC-miR-20a. Methods: Bioinformatic analysis predicted that porcine LDLR is a target of SSC-miR-20a. Wild-type and mutant LDLR 3′-untranslated region (UTR) fragments were generated by polymerase chain reaction (PCR) and cloned into the pGL3-Control vector to construct pGL3 Control LDLR wild-3′-UTR and pGL3 Control LDLR mutant-3′-UTR recombinant plasmids, respectively. An miR-20a expression plasmid was constructed by inserting the porcine pre-miR-20a-coding sequence between the HindIII and BamHI sites in pMR-mCherry, and constructs were confirmed by sequencing. HEK293T cells were co-transfected with the miR-20a expression or pMR-mCherry control plasmids and constructs harboring the corresponding 3′-UTR, and relative luciferase activity was determined. The relative expression levels of miR-20a and LDLR mRNA and their correlation in terms of expression levels in porcine liver tissue were analyzed using reverse-transcription quantitative PCR. Results: Gel electrophoresis and sequencing showed that target gene fragments were successfully cloned, and the three recombinant vectors were successfully constructed. Compared to pMR-mCherry, the miR-20a expression vector significantly inhibited wild-type LDLR-3′-UTR-driven (p<0.01), but not mutant LDLR-3′-UTR-driven (p>0.05), luciferase reporter activity. Further, miR-20a and LDLR were expressed at relatively high levels in porcine liver tissues. Pearson correlation analysis revealed that porcine liver miR-20a and LDLR levels were significantly negatively correlated (r = –0.656, p<0.05). Conclusion: LDLR is a potential target of miR-20a, which might directly bind the LDLR 3′-UTR to post-transcriptionally inhibit expression. These results have implications in understanding the pathogenesis and progression of porcine cardiovascular diseases.

Lane-Change Collision Avoidance Control for Automated Vehicles with Control Barrier Functions

Ding Yang,Zhong Hong,Qian Yahui,Wang Liangmo,Xie Yuan 한국자동차공학회 2023 International journal of automotive technology Vol.24 No.3

In congested street or highway scenarios, such as lane-change in dynamically changing traffic flow situations, the planning and tracking of trajectories for connected and automated vehicles (CAVs) represent some of the most challenging tasks. As an introduction to automated lane-change in CAVs, this paper presents a control Lyapunov function (CLF) approach that follows an optimal desired trajectory while observing the constraints imposed by the control barrier function (CBF) in order to avoid collision with surrounding vehicles. By combining CLF and CBF within the framework of quadratic programs (QP), it allows the implementation to simultaneously track the control objective (represented by the CLF) and satisfy the constraints of the desired state of the system (represented by the CBF). Therefore, it provides the possibility of tracking simultaneously the path of the unmanned vehicle, within the constraints of the surrounding vehicles as well as the surrounding environment. From simulations and comparison results, the controller presented here can perform collision avoidance well and can be used on a real traffic system, which has the advantage of providing faster and more precise lane-change results than another work.

Immunosuppression and Neuroinflammation in Stroke Pathobiology

Qian Jiang,Christopher R. Stone,Kenneth Elkin,Xiaokun Geng,Yuchuan Ding 한국뇌신경과학회 2021 Experimental Neurobiology Vol.30 No.2

Over the preceding decades, there have been substantial advances in our knowledge of the pathophysiology of stroke. One such advance has been an increased understanding of the multifarious crosstalk in which the nervous and immune systems engage in order to maintain homeostasis. By interrupting the immune-nervous nexus, it is thought that stroke induces change in both systems. Additionally, it has been found that both innate and adaptive immunosuppression play protective roles against the effects of stroke. The release of danger-/damage-associated molecular patterns (DAMPs) activates Toll-like receptors (TLRs), contributing to the harmful inflammatory effects of ischemia/reperfusion injury after stroke; the Tyro3, Axl, and MerTK (TAM)/Gas6 system, however, has been shown to suppress inflammation via downstream signaling molecules that inhibit TLR signaling. Anti-inflammatory cytokines have also been found to promote neuroprotection following stroke. Additionally, adaptive immunosuppression merits further consideration as a potential endogenous protective mechanism. In this review, we highlight recent studies regarding the effects and mechanism of immunosuppression on the pathophysiology of stroke, with the hope that a better understanding of the function of both of innate and adaptive immunity in this setting will facilitate the development of effective therapies for post-stroke inflammation.