TY - JOUR
T1 - Identification and expression analysis of 26 oncogenes of the receptor tyrosine kinase family in channel catfish after bacterial infection and hypoxic stress
AU - Tian, Yi
AU - Yao, Jun
AU - Liu, Shikai
AU - Jiang, Chen
AU - Zhang, Jiaren
AU - Li, Yun
AU - Feng, Jianbin
AU - Liu, Zhanjiang
N1 - Publisher Copyright:
© 2015 Elsevier Inc. All rights reserved.
PY - 2015/6
Y1 - 2015/6
N2 - Receptor tyrosine kinases (RTKs) are high-affinity cell surface receptors for many polypeptide growth factors, cytokines and hormones. RTKs are not only key regulators of normal cellular processes, but are also involved in the progression of many types of tumors, and responses to various biotic and abiotic stresses. Catfish is a primary aquaculture species in the United States, while its industry is drastically hindered by several major diseases including enteric septicemia of catfish (ESC) that is caused by Edwardsiella ictaluri. Disease outbreaks are often accompanied by hypoxic stress, which affects the performance and survival of fish by reducing disease resistance. In this study, we identified 26 RTK oncogenes in the channel catfish genome, and determined their expression profiles after ESC infection and hypoxic stress. The 26 RTK genes were divided into four subfamilies according to phylogenetic analysis, including TIE (2 genes), ErbB (6 genes), EPH (14 genes), and INSR (4 genes). All identified RTKs possess a similar molecular architecture including ligand-binding domains, a single transmembrane helix and a cytoplasmic region, which suggests that these genes could play conserved biological roles. The expression analysis revealed that eight RTKs were significantly regulated after bacterial infection, with dramatic induction of insulin receptor genes including INSRb, IGF1Ra, and IGF1Rb. Upon hypoxic stress, EPHB3a, EGFR, ErbB4b, and IGF1Rb were expressed at higher levels in the tolerant catfish, while EPHA2a, EPHA2, TIE1 and INSRa were expressed at higher levels in the intolerant catfish. These results suggested the involvement of RTKs in immune responses and hypoxic tolerance.
AB - Receptor tyrosine kinases (RTKs) are high-affinity cell surface receptors for many polypeptide growth factors, cytokines and hormones. RTKs are not only key regulators of normal cellular processes, but are also involved in the progression of many types of tumors, and responses to various biotic and abiotic stresses. Catfish is a primary aquaculture species in the United States, while its industry is drastically hindered by several major diseases including enteric septicemia of catfish (ESC) that is caused by Edwardsiella ictaluri. Disease outbreaks are often accompanied by hypoxic stress, which affects the performance and survival of fish by reducing disease resistance. In this study, we identified 26 RTK oncogenes in the channel catfish genome, and determined their expression profiles after ESC infection and hypoxic stress. The 26 RTK genes were divided into four subfamilies according to phylogenetic analysis, including TIE (2 genes), ErbB (6 genes), EPH (14 genes), and INSR (4 genes). All identified RTKs possess a similar molecular architecture including ligand-binding domains, a single transmembrane helix and a cytoplasmic region, which suggests that these genes could play conserved biological roles. The expression analysis revealed that eight RTKs were significantly regulated after bacterial infection, with dramatic induction of insulin receptor genes including INSRb, IGF1Ra, and IGF1Rb. Upon hypoxic stress, EPHB3a, EGFR, ErbB4b, and IGF1Rb were expressed at higher levels in the tolerant catfish, while EPHA2a, EPHA2, TIE1 and INSRa were expressed at higher levels in the intolerant catfish. These results suggested the involvement of RTKs in immune responses and hypoxic tolerance.
KW - Disease infection
KW - Expression
KW - Fish
KW - Hypoxic stress
KW - RTKs
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U2 - 10.1016/j.cbd.2015.02.001
DO - 10.1016/j.cbd.2015.02.001
M3 - Article
C2 - 25722053
AN - SCOPUS:84923352309
SN - 1744-117X
VL - 14
SP - 16
EP - 25
JO - Comparative Biochemistry and Physiology - Part D: Genomics and Proteomics
JF - Comparative Biochemistry and Physiology - Part D: Genomics and Proteomics
ER -