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The genome of the mesopolyploid crop species Brassica rapa
Wang, Xiaowu,Wang, Hanzhong,Wang, Jun,Sun, Rifei,Wu, Jian,Liu, Shengyi,Bai, Yinqi,Mun, Jeong-Hwan,Bancroft, Ian,Cheng, Feng,Huang, Sanwen,Li, Xixiang,Hua, Wei,Wang, Junyi,Wang, Xiyin,Freeling, Michael Nature Publishing Group, a division of Macmillan P 2011 Nature genetics Vol.43 No.10
We report the annotation and analysis of the draft genome sequence of Brassica rapa accession Chiifu-401-42, a Chinese cabbage. We modeled 41,174 protein coding genes in the B. rapa genome, which has undergone genome triplication. We used Arabidopsis thaliana as an outgroup for investigating the consequences of genome triplication, such as structural and functional evolution. The extent of gene loss (fractionation) among triplicated genome segments varies, with one of the three copies consistently retaining a disproportionately large fraction of the genes expected to have been present in its ancestor. Variation in the number of members of gene families present in the genome may contribute to the remarkable morphological plasticity of Brassica species. The B. rapa genome sequence provides an important resource for studying the evolution of polyploid genomes and underpins the genetic improvement of Brassica oil and vegetable crops.
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Dihydroartemisinin inhibits HepG2.2.15 proliferation by inducing cellular senescence and autophagy
( Jiang Zou ),( Qiang Ma ),( Ru Sun ),( Jiajing Cai ),( Hebin Liao ),( Lei Xu ),( Jingruo Xia ),( Guangcheng Huang ),( Lihua Yao ),( Yan Cai ),( Xiaowu Zhong ),( Xiaolan Guo ) 생화학분자생물학회 2019 BMB Reports Vol.52 No.8
Dihydroartemisinin (DHA) has been reported to possess anti-cancer activity against many cancers. However, the pharmacologic effect of DHA on HBV-positive hepatocellular carcinoma (HCC) remains unknown. Thus, the objective of the present study was to determine whether DHA could inhibit the proliferation of HepG2.2.15 cells and uncover the underlying mechanisms involved in the effect of DHA on HepG2.2.15 cells. We found that DHA effectively inhibited HepG2.2.15 HCC cell proliferation both in vivo and in vitro. DHA also reduced the migration and tumorigenicity capacity of HepG2.2.15 cells. Regarding the underlying mechanisms, results showed that DHA induced cellular senescence by up-regulating expression levels of proteins such as p-ATM, p-ATR, γ-H<sub>2</sub>AX, P53, and P21 involved in DNA damage response. DHA also induced autophagy (green LC3 puncta gathered together and LC3II/LC3I ratio increased through AKT-mTOR pathway suppression). Results also revealed that DHA-induced autophagy was not linked to senescence or cell death. TPP1 (telomere shelterin) overexpression could not rescue DHA-induced anticancer activity (cell proliferation). Moreover, DHA down-regulated TPP1 expression. Gene knockdown of TPP1 caused similar phenotypes and mechanisms as DHA induced phenotypes and mechanisms in HepG2.2.15 cells. These results demonstrate that DHA might inhibit HepG2.2.15 cells proliferation through inducing cellular senescence and autophagy. [BMB Reports 2019; 52(8): 520-525]
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