Identification and genetic mapping for rht-DM, a dominant dwarfing gene in mutant semi-dwarf maize using QTL-seq approach

Qian Chen,Jun Song,Wen‑Ping Du,Li‑Yuan Xu,Yun Jiang,Jie Zhang,Xiao‑Li Xiang,Gui‑Rong Yu 한국유전학회 2018 Genes & Genomics Vol.40 No.10

Semi-dwarfism is an agronomically important trait in breeding for stable high yields and for resistance to damage by wind and rain (lodging resistance). Many QTLs and genes causing dwarf phenotype have been found in maize. However, because of the yield loss associated with these QTLs and genes, they have been difficult to use in breeding for dwarf stature in maize. Therefore, it is important to find the new dwarfing genes or materials without undesirable characters. The objectives of this study were: (1) to figure out the inheritance of semi-dwarfism in mutants; (2) mapping dwarfing gene or QTL. Maize inbred lines ‘18599’ and ‘DM173’, which is the dwarf mutant derived from the maize inbred line ‘173’ through 60Co-γ ray irradiation. F2 and BC1F1 population were used for genetic analysis. Whole genome resequencing-based technology (QTL-seq) were performed to map dwarfing gene and figured out the SNP markers in predicted region using dwarf bulk and tall bulk from F2 population. Based on the polymorphic SNP markers from QTL-seq, we were fine-mapping the dwarfing gene using F2 population. In F2 population, 398 were dwarf plants and 135 were tall plants. Results of χ2 tests indicated that the ratio of dwarf plants to tall plants was fitted to 3:1 ratio. Furthermore, the χ2 tests of BC1F1 population showed that the ratio was fitted to 1:1 ratio. Based on QTL-seq, the dwarfing gene was located at the region from 111.07 to 124.56 Mb of chromosome 9, and we named it rht-DM. Using traditional QTL mapping with SNP markers, the rht-DM was narrowed down to 400 kb region between SNP-21 and SNP-24. The two SNPs were located at 0.43 and 0.11 cM. Segregation analysis of F2 and BC1F1 indicated that the dwarfing gene was likely a dominant gene. This dwarfing gene was located in the region between 115.02 and 115.42 Mb on chromosome 9.

Dynamic analysis for gene expression profiles of endothelial colony forming cells under hypoxia

De-Cai Yu,Wen-Du Feng,Xian-Biao Shi,hi-Yong Wang,Wei Ge,Chun-Ping Jiang,Xi-Tai Sun,Yi-Tao Ding 한국유전학회 2013 Genes & Genomics Vol.35 No.4

Previous studies have shown that endothelial colony forming cells (ECFCs) play an important role in the neovascularization of tumors. Hypoxia is emphasized as an important promoter of angiogenesis. However, little is known about genome-wide transcriptional regulation of ECFCs under hypoxic conditions. In this study, gene expression profiles in ECFCswere evaluated under hypoxic conditions for 3, 6, 12, 24,and 48 h, using Affymetrix U133 plus 2.0 chip microarray. 1,103 hypoxia-regulated genes were filtered, with 379(0.693 %) genes up-regulated and 724 (1.32 %) genes downregulated. Most of the up-regulated genes were involved in apoptosis, cell proliferation, or metabolic processes, while most of the down-regulated genes were involved in cell adherence,cell cycle,DNAandmRNAmetabolic processes,multi-cellular organism development, protein metabolic processes, response to stress, signal transduction, or transport. This expression profile is ECFC-specific, because it is significantly different from those of endothelial cells and smooth muscle cells under hypoxic conditions. Moreover, hypoxia-regulated apoptosis in ECFCs is mainly related with the mitochondrial pathway (p53-BAX-Caspase-9) and the death receptor pathway (FASCaspase-8-Caspase-3). MAPK pathway is activated in ECFCs under hypoxic conditions. The differentially expressed genes of ECFCs were identified under hypoxic conditions, and related with cell apoptosis, cell cycle and MAPK pathways, shedding light on the mechanism of angiogenesis.

Post-fire Study on Mechanical Properties of Damaged Ultra-high Strength Concrete

Xiao Lyu,Guang-Hao Jia,Gan-Ping Shu,Xin Zhang,Er-Feng Du,Wen-Ming Wang 한국강구조학회 2022 International Journal of Steel Structures Vol.22 No.6

In order to study the eff ect of steel tube, pre-load and temperature on residual performance of heated ultra-high strength concrete (UHSC), an experimental program was carried out to investigate the physical and mechanical properties of UHSC post-fi re in room temperature. With total of 54 standard cylindrical concrete specimens subjected to various temperatures ranging from 62 °C to 496 °C, their residual compressive strength, elastic modulus, peak strain was measured after natural cooling down. By comparing the test results of standard cylindrical concrete specimens with the results of the bare specimens in and after fi re, it is known that the residual compressive strength of standard cylindrical concrete specimens decayed more serious after exposing to same temperature. Seen from the results, the temperature which the specimens suff ered was found to be responsibility to the reduction of the compressive strength, elastic modulus, peak strain. As the temperature up to 300 °C, the strength reduction coeffi cient of UHSC was 0.67 ~ 0.68 and the elastic modulus reduction coeffi cient of UHSC was 0.41 ~ 0.51 with peak strain coeffi cient ε cr ( T ) /ε 0 1.57 ~ 1.67. Finally, based on the analysis of test results, simple formulae were proposed to describe the eff ect of temperature on residual performance of heated UHSC which infi lled the steel tube.

Simultaneous Determination of Hydroquinone and Catechol by N-doped Porous Biochar-modified Electrode

Yue-Xin Liu,Shi-Man Du,Jie Cao,Wen-sheng Huang,Xiao-Ru Zhang,Bao-Ping Qi,Sheng-Hui Zhang 대한화학회 2020 Bulletin of the Korean Chemical Society Vol.41 No.3

N-doped porous biochar (NPB) with large conjugated systems could not only be used as enrichment carriers but also be in favor of electron transport in the electrochemical detection. The NPB-modified electrode was fabricated for the simultaneous detection of catechol (CA) and hydroquinone (HQ) to enhance the signal-to-noise ratio and further improve the sensitivity. A detection limit as low as 37 and 47?nM was achieved for CA and HQ, respectively. The proposed strategy with the merits of high sensitivity, selectivity, and reproducibility exhibited a great potential for the detection.

Tug of War-Who is the Winner? Canker Disease Restructures the Endophytic Bacterial Community of Citrus

Jian-Yu Zhou,Yi Zhang,Wen-Ping Xu,Misbah Naz,Xiao-Meng Li,Xu Li,Bi-Ying Zhao,Shan-Shan Qi,Zhi-Cong Dai,Dao-Lin Du 한국원예학회 2023 원예과학기술지 Vol.41 No.5

Toxic Epidermal Necrolysis Induced by Sintilimab: A Case Report

Ya-lei Lye,Bin Shan,Chen-hong Jia,Jiang Liu,Juan Hou,Wen-li Du,Rui Feng,Ping Liang 대한피부과학회 2023 Annals of Dermatology Vol.35 No.-

Sintilimab is an anti-programmed cell death receptor-1 antibody. The phase III clinical trial ORIENT-12 confirmed the safety of sintilimab combined with pemetrexed/platinum in the treatment of advanced squamous non-small cell lung cancer. Skin reactions are the most commonly reported adverse events of immune checkpoint inhibitors and are rarely severe. We describe a case of toxic epidermal necrolysis related to sintilimab in an elderly oncologic patient. 3 weeks after immunotherapy, the patient developed an extensive rash and diffuse itching, rapidly evolving into macules, blisters, bullae and erosions. Causal evaluation was performed based on the algorithm of drug causality for epidermal necrolysis and national Food and Drug Administration qualitative analysis. The patient responded to high-dose glucocorticosteroid and supportive therapy, alongside with local wound care. If immune checkpoint inhibitors need to be extrapolated clinically, strictly following evidence-based research, promptly detecting and treating adverse reactions is crucial.

β-elemene Induces Caspase-dependent Apoptosis in Human Glioma Cells in vitro through the Upregulation of Bax and Fas/FasL and Downregulation of Bcl-2

Li, Chen-Long,Chang, Liang,Guo, Lin,Zhao, Dan,Liu, Hui-Bin,Wang, Qiu-Shi,Zhang, Ping,Du, Wen-Zhong,Liu, Xing,Zhang, Hai-Tao,Liu, Yang,Zhang, Yao,Xie, Jing-Hong,Ming, Jian-Guang,Cui, Yu-Qiong,Sun, Ying Asian Pacific Journal of Cancer Prevention 2014 Asian Pacific journal of cancer prevention Vol.15 No.23

Background: ${\beta}$-elemene, extracted from herb medicine Curcuma wenyujin has potent anti-tumor effects in various cancer cell lines. However, the activity of ${\beta}$-elemene against glioma cells remains unclear. In the present study, we assessed effects of ${\beta}$-elemene on human glioma cells and explored the underlying mechanism. Materials and Methods: Human glioma U87 cells were used. Cell proliferation was determined with MTT assay and colony formation assay to detect the effect of ${\beta}$-elemene at different doses and times. Fluorescence microscopy was used to observe cell apoptosis with Hoechst 33258 staining and change of glioma apoptosis and cell cycling were analyzed by flow cytometry. Real-time quantitative PCR and Western-blotting assay were performed to investigated the influence of ${\beta}$-elemene on expression levels of Fas/FasL, caspase-3, Bcl-2 and Bax. The experiment was divided into two groups: the blank control group and ${\beta}$-elemne treatment group. Results: With increase in the concentration of ${\beta}$-elemene, cytotoxic effects were enhanced in the glioma cell line and the concentration of inhibited cell viability ($IC_{50}$) was $48.5{\mu}g/mL$ for 24h. ${\beta}$-elemene could induce cell cycle arrest in the G0/G1 phase. With Hoechst 33258 staining, apoptotic nuclear morphological changes were observed. Activation of caspase-3,-8 and -9 was increased and the pro-apoptotic factors Fas/FasL and Bax were upregulated, while the anti-apoptotic Bcl-2 was downregulated after treatment with ${\beta}$-elemene at both mRNA and protein levels. Furthermore, proliferation and colony formation by U87 cells were inhibited by ${\beta}$-elemene in a time and does-dependent manner. Conclusions: Our results indicate that ${\beta}$-elemene inhibits growth and induces apoptosis of human glioma cells in vitro. The induction of apoptosis appears to be related with the upregulation of Fas/FasL and Bax, activation of caspase-3,-8 and -9 and downregulation of Bcl-2, which then trigger major apoptotic cascades.