Characterization and expression analysis of TNF-related apoptosis inducing ligand (TRAIL) in grass carp Ctenopharyngodon idella

被引:21
作者
Chang, MX
Nie, P [1 ]
Xie, HX
Wang, GL
Gao, Y
机构
[1] Chinese Acad Sci, Inst Hydrobiol, State Key Lab Freshwater Ecol & Biotechnol, Wuhan 430072, Hubei Province, Peoples R China
[2] Chinese Acad Sci, Inst Hydrobiol, Lab Fish Dis, Wuhan 430072, Hubei Province, Peoples R China
基金
中国国家自然科学基金;
关键词
TRAIL; genome; promoter; expression; grass carp;
D O I
10.1016/j.vetimm.2005.09.003
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 ;
摘要
TRAIL (Apo2 ligand) described as a type II transmembrame protein belonging to the TNF superfamily can induce apoptotic cell death in a variety of cell types. In the present study, a putative cDNA sequence encoding the 299 amino acids of TRAIL (GC-TRAIL) and its genomic organization were identified in grass carp Ctenopharyngodon idella. The predicted GC-TRAIL sequence showed 44 and 41% identities to chicken and human TRAILs, respectively. In a domain search, a tumor necrosis factor homology domain (THD) was identified in the C-terminal portion of TRAILs. The GC-TRAIL gene consists of five exons, with four intervening introns, spaced over approximately 4 kb of genomic sequence. Analysis of GC-TRAlL promoter region revealed the presence of a number of putative transcription factor binding sites, such as Sp1, NF-kappaB, AP-1, GATA, NFAT, HNF, STAT, P53 and IRFI sequences which are important for the expression of other TNF family members. Phylogenetic analysis placed GC-TRAIL and the putative zebrafish (Danio rerio) TRAIL obtained from searching the zebrafish database into one separate cluster near mammalian TRAIL genes, but apart from the reported zebrafish TRAIL-like protein, indicating that the GC-TRAIL is an authentic fish TRAIL. Expression analysis revealed that GC-TRAIL is expressed in many tissues, such as in gills, liver, trunk kidney, head kidney, intestine and spleen. (c) 2005 Elsevier B.V. All rights reserved.
引用
收藏
页码:51 / 63
页数:13
相关论文
共 22 条
[1]   Cloning and characterization of chicken tumor necrosis factor (TNF)-superfamily ligands, CD30L and TNF-related apoptosis inducing ligand (TRAIL) [J].
AbdallA, SA ;
Horiuchi, H ;
Furusawa, S ;
Matsuda, H .
JOURNAL OF VETERINARY MEDICAL SCIENCE, 2004, 66 (06) :643-650
[2]   Disruption of NF-κB signaling reveals a novel role for NF-κB in the regulation of TNF-related apoptosis-inducing ligand expression [J].
Baetu, TM ;
Kwon, H ;
Sharma, S ;
Grandvaux, N ;
Hiscott, J .
JOURNAL OF IMMUNOLOGY, 2001, 167 (06) :3164-3173
[3]   Molecular cloning and expression of a TNF receptor and two TNF ligands in the fish ovary [J].
Bobe, J ;
Goetz, FW .
COMPARATIVE BIOCHEMISTRY AND PHYSIOLOGY B-BIOCHEMISTRY & MOLECULAR BIOLOGY, 2001, 129 (2-3) :475-481
[4]  
Choi EA, 2003, CANCER RES, V63, P5299
[5]   Genomic organization and transcriptional regulation of human Apo2/TRAIL gene [J].
Gong, B ;
Almasan, A .
BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS, 2000, 278 (03) :747-752
[6]   FAS LIGAND-INDUCED APOPTOSIS AS A MECHANISM OF IMMUNE PRIVILEGE [J].
GRIFFITH, TS ;
BRUNNER, T ;
FLETCHER, SM ;
GREEN, DR ;
FERGUSON, TA .
SCIENCE, 1995, 270 (5239) :1189-1192
[7]   Roles of TNF-related apoptosis-inducing ligand in experimental autoimmune encephalomyelitis [J].
Hilliard, B ;
Wilmen, A ;
Seidel, C ;
Liu, TST ;
Göke, R ;
Chen, YH .
JOURNAL OF IMMUNOLOGY, 2001, 166 (02) :1314-1319
[8]   Apoptosis induced in normal human hepatocytes by tumor necrosis factor-related apoptosis-inducing ligand [J].
Jo, M ;
Kim, TH ;
Seol, DW ;
Esplen, JE ;
Dorko, K ;
Billiar, TR ;
Strom, SC .
NATURE MEDICINE, 2000, 6 (05) :564-567
[9]   Regulation of Fas-ligand expression during activation-induced cell death in T lymphocytes via nuclear factor κB [J].
Kasibhatla, S ;
Genestier, L ;
Green, DR .
JOURNAL OF BIOLOGICAL CHEMISTRY, 1999, 274 (02) :987-992
[10]   Type I interferons (IFNs) regulate tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) expression on human T cells: A novel mechanism for the antitumor effects of type IIFNs [J].
Kayagaki, N ;
Yamaguchi, N ;
Nakayama, M ;
Eto, H ;
Okumura, K ;
Yagita, H .
JOURNAL OF EXPERIMENTAL MEDICINE, 1999, 189 (09) :1451-1460