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| 1 | Development and utilization of a new chemically-induced soybean library with a high mutation density显示文摘Mutagenized populations have provided important materials for introducing variation and identifying gene function in plants. In this study, an ethyl methanesulfonate(EMS)-induced soybean(Glycine max) population,consisting of 21,600 independent M_2 lines, was developed.Over 1,000 M_(4(5))families, with diverse abnormal phenotypes for seed composition, seed shape, plant morphology and maturity that are stably expressed across different environments and generations were identified. Phenotypic analysis of the population led to the identification of a yellow pigmentation mutant, gyl, that displayed significantly decreased chlorophyll(Chl) content and abnormal chloroplast development. Sequence analysis showed that gyl is allelic to Minn Gold, where a different single nucleotide polymorphism variation in the Mg-chelatase subunit gene(ChlI1a) results in golden yellow leaves. A cleaved amplified polymorphic sequence marker was developed and may be applied to marker-assisted selection for the golden yellow phenotype in soybean breeding. We show that the newly developed soybean EMS mutant population has potential for functional genomics research and genetic improvement in soybean. | Zhongfeng Li Lingxue Jiang Yansong Ma Zhongyan Wei Huilong Hong Zhangxiong Liu Jinhui Lei Ying Liu Rongxia Guan Yong Guo Longguo Jin Lijuan Zhang Yinghui Li Yulong Ren Wei He Ming Liu Nang Myint Phyu Sin Htwe Lin Liu Bingfu Guo Jian Song Bing Tan Guifeng Liu Maiquan Li Xianli Zhang Bo Liu Xuehui Shi Sining Han Sunan Hua Fulai Zhou Lili Yu Yanfei Li Shuang Wang Jun Wang Ruzhen Chang Lijuan Qiu | 2017 | Journal of Integrative Plant Biology2017，59，1： | 6 |
| 2 | High resolution, structural studies of a pyrolytic carbon used in medical applications 显示文摘 | Ma L Sines G | 2002 | Carbon2002，40，3： | 1 |
| 3 | JUNB mediates oxaliplatin resistance via the MAPK signaling pathway in gastric cancer by chromatin accessibility and transcriptomic analysis显示文摘tients,and chemotherapy resistance is one of the main reasons for treatment failure.Thus,it is important to reveal the mechanism of oxaliplatin resistance and to seek effective intervention strategies to improve chemotherapy sensitivity,thereby improving the survival and prognosis of gastric cancer patients.To understand the molecular mechanisms of oxaliplatin resistance,we generate an oxaliplatin-resistant gastric cancer cell line and conduct assay for transposase-accessible chromatin sequencing(ATAC-seq)and RNA sequencing(RNA-seq)for both parental and oxaliplatin-resistant AGS cells.A total of 3232 genomic regions are identified to have higher accessibility in ox-aliplatin-resistant cells,and DNA-binding motif analysis identifies JUNB as the core transcription factor in the regulatory network.JUNB is overexpressed in oxaliplatin-resistant gastric cancer cells,and its upregulation is associated with poor prognosis in gastric cancer patients,which is validated by our tissue microarray data.Moreover,chromatin immunoprecipitation sequencing(ChIP-seq)analysis reveals that JUNB binds to the tran-scriptional start site of key genes involved in the MAPK signaling pathway.Knockdown of JUNB inhibits the MAPK signaling pathway and restores sensitivity to oxaliplatin.Combined treatment with the ERK inhibitor piperlongu-mine or MEK inhibitor trametinib effectively overcomes oxaliplatin resistance.This study provides evidence that JUNB mediates oxaliplatin resistance in gastric cancer by activating the MAPK pathway.The combination of MAPK inhibitors with oxaliplatin overcomes resistance to oxaliplatin,providing a promising treatment opportunity for oxaliplatin-resistant gastric cancer patients. | Suyao Li Yichou Wei Xun Sun Mengling Liu Mengxuan Zhu Yitao Yuan Jiayu Zhang Yu Dong Keshu Hu Sining Ma Xiuping Zhang Bei Xu Hesheng Jiang Lu Gan Tianshu Liu | 2023 | Acta Biochimica et Biophysica Sinica2023，55，11： | 0 |
| 4 | Negative correlation between acetyl-CoA acyltransferase 2 and cetuximab resistance in colorectal cancer显示文摘The emergence of anti-EGFR therapy has revolutionized the treatment of colorectal cancer(CRC).However,not all patients respond consistently well.Therefore,it is imperative to conduct further research to identify the molecular mechanisms underlying the development of cetuximab resistance in CRC.In this study,we find that the expressions of many metabolism-related genes are downregulated in cetuximab-resistant CRC cells compared to their sensitive counterparts.Specifically,acetyl-CoA acyltransferase 2(ACAA2),a key enzyme in fatty acid metabolism,is downregulated during the development of cetuximab resistance.Silencing of ACAA2 promotes proliferation and increases cetuximab tolerance in CRC cells,while overexpression of ACAA2 exerts the opposite effect.RTK-Kras signaling might contribute to the downregulation of ACAA2 expression in CRC,and ACAA2 predicts CRC prognosis in patients with Kras mutations.Collectively,our data suggest that modulating ACAA2 expression contributes to secondary cetuximab resistance in Kras wild-type CRC patients.ACAA2 expression is related to Kras mutation and demonstrates a prognostic role in CRC patients with Kras mutation.Thus,ACAA2 is a potential target in CRC with Kras mutation. | Yitao Yuan Xun Sun Mengling Liu Suyao Li Yu Dong Keshu Hu Jiayu Zhang Bei Xu Sining Ma Hesheng Jiang Pengcong Hou Yufu Lin Lu Gan Tianshu Liu | 2023 | Acta Biochimica et Biophysica Sinica2023，55，9： | 0 |
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