Molecular Characterization and Response of Silver Carp (Hypophthalmichthys molitrix) GLUT1 under Hypoxia Stress
文献类型： 外文期刊
作者： Zhang, Zewen 1 ; Li, Xiaohui 1 ; Zou, Guiwei 1 ; Liang, Hongwei 1 ;
作者机构： 1.Chinese Acad Fishery Sci, Yangtze River Fisheries Res Inst, Wuhan 430223, Peoples R China
2.Hebei Univ, Inst Life Sci & Green Dev, Hebei Basic Sci Ctr Biot Interact, Sch Life Sci, Baoding 071002, Peoples R China
3.Huazhong Agr Univ, Hubei Hongshan Lab, Wuhan 430070, Peoples R China
关键词： glucose transporter 1; Hypophthalmichthys molitrix; hypoxia stress; glucose metabolism
期刊名称：FISHES （ 影响因子：2.3； 五年影响因子：2.4 ）
ISSN：
年卷期： 2023 年 8 卷 8 期
页码：
收录情况： SCI
摘要： As an important freshwater species with economic and ecological benefits, silver carp (Hypophthalmichthys molitrix) exhibits poor tolerance to hypoxia. Glucose transporters (GLUTs) are core membrane proteins that transport glucose to tissues and regulate essential life activities. Its expression is regulated by HIF-1a and cells in hypoxic conditions to maintain energy demand through GLUTs inducing enhanced glucose transport. We cloned H. molitrix glut1 (SLC2A1) and analyzed its sequence using bioinformatics tools. The glut1 cDNA was 2104 base pairs long and encoded a 490 amino acid protein. Phylogenetic analysis revealed that sliver carp glut1 is evolutionarily conserved and exhibited the highest sequence similarity with Ctenopharyngodon idella glut1. Glut1 expression was the highest and lowest in the gills and liver, respectively. Hypoxic stress significantly increased glut1 expression in the brain (p < 0.05); in the gills, it was the highest and lowest in the semi-asphyxia and asphyxia groups, respectively; in the liver, it was significantly higher under hypoxia than that of the normoxia group; and in the heart, it was significantly higher in the floating head, semi-asphyxia, and asphyxia groups than in the normoxia group (p < 0.05). The proposed mechanism may thus provide the basis for elucidating the molecular basis of silver carp's hypoxia stress response mediated by glut1.
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