fbxo32基因在traf6缺失斑马鱼肝脏中的表达分析  

THE EXPRESSION ANALYSIS OF FBXO32 GENE IN LIVER OF TRAF6 MUTANT ZEBRAFISH

作　　者：吴士培 欧密 李凯彬[2] 许巧情[1] 徐红艳 WU Shi-Pei;OU Mi;LI Kai-Bin;XU Qiao-Qing;XU Hong-Yan(College of Animal Sciences,Yangtze University,Jingzhou 434025,China;Key Laboratory of Tropical&Subtropical Fishery Resource Application&Cultivation,Ministry of Agriculture,Pearl River Fisheries Research Institute,Chinese Academy of Fishery Sciences,Guangzhou 510380,China;Key Laboratory of Freshwater Fish Reproduction and Development,Ministry of Education,College of Fisheries,Southwest University,Chongqing 400715,China)

机构地区：[1]长江大学动物科学学院,荆州434025 [2]中国水产科学研究院珠江水产研究所,农业农村部热带亚热带水产资源利用与养殖重点实验室,广州510380 [3]西南大学水产学院,淡水鱼类资源与生殖发育教育部重点实验室,重庆400715

出　　处：《水生生物学报》2021年第5期945-950,共6页Acta Hydrobiologica Sinica

基　　金：广东省自然科学基金(2018A030310054)资助。

摘　　要：为了进一步研究fbxo32在肝脏相关疾病中的作用,进行了traf6缺失斑马鱼Danio rerio肝脏的组织切片分析,结果显示斑马鱼traf6缺失个体表现出明显的肝萎缩特征,包括肝脏组织结构松散、肝细胞排列不规则及缺少肝脂肪滴等症状。同时荧光定量实验表明fbxo32 mRNA在检测过的野生型斑马鱼组织中均有一定量的表达,在肝脏中表达量较低而在卵巢中表达量较高。而与野生型斑马鱼相比,fbxo32 mRNA在traf6突变体斑马鱼肝脏中的表达量上调超过100倍。进一步原位杂交结果显示,fbxo32 mRNA的信号主要集中于肝脏细胞,而在血细胞中则没有检测到信号。特别是与野生型斑马鱼相比,fbxo32 mRNA在traf6突变型斑马鱼肝脏中的信号明显增强。实验结果表明traf6缺失能引起fbxo32基因的上调表达,并会导致traf6突变型斑马鱼肝脏发育异常并发生萎缩。fbxo32,a muscle-specific E3 ubiquitin ligase,can enhance protein degradation to associate with atrophy.Here,we found that traf6 mutant zebrafish liver fbxo32 mRNA level increased dramatically.To find out the role of fbxo32 in liver disease,we performed histological analysis of mutant and wildtype zebrafish liver.The result showed that the mutant liver exhibited apparent characteristics of liver atrophy,such as loose liver tissue structure,irregular arrangement and rare lipid droplets of the hepatocytes.The qRT-PCR result showed that fbxo32 mRNA was widely expressed in most tested tissues with the highest level in ovary and low level in liver of wildtype zebrafish.Especially,compared with the wildtype,the liver fbxo32 mRNA was elevated about 100 folds in the traf6 mutant.Additionally,fbxo32 mRNA was mainly distributed in hepatocytes based on in situ hybridization,but cannot be detected in blood cells.The signal of fbxo32 mRNA was much stronger in traf6 mutant liver.These findings indicate that the knockout of traf6 might induce the expression of fbxo32 mRNA in liver and result in liver developmental abnormality and atrophy.

关 键 词：肝脏萎缩 fbxo32 traf6突变体 原位杂交 斑马鱼 

分 类 号：Q344.1[生物学—遗传学]