ZFIN ID: ZDB-PUB-020701-9
Structure, developmental expression, and physiological regulation of zebrafish IGF binding protein-1
Maures, T.J. and Duan, C.
Date: 2002
Source: Endocrinology   143(7): 2722-2731 (Journal)
Registered Authors: Duan, Cunming
Keywords: none
MeSH Terms:
  • Amino Acid Sequence
  • Animals
  • Base Sequence
  • Blotting, Northern
  • Cloning, Molecular
  • Databases, Factual
  • Embryo, Nonmammalian
  • Gene Expression Regulation, Developmental/physiology*
  • Hypoxia/metabolism
  • In Situ Hybridization
  • Insulin-Like Growth Factor Binding Protein 1/biosynthesis*
  • Insulin-Like Growth Factor Binding Protein 1/genetics*
  • Insulin-Like Growth Factor Binding Protein 1/physiology
  • Liver/embryology
  • Liver/metabolism
  • Molecular Sequence Data
  • Nutritional Physiological Phenomena
  • RNA, Messenger/biosynthesis
  • RNA, Messenger/genetics
  • Reverse Transcriptase Polymerase Chain Reaction
  • Tissue Distribution
  • Zebrafish
PubMed: 12072407 Full text @ Endocrinology
ABSTRACT
The biological activity and availability of IGFs are regulated by a group of secreted proteins that belong to the IGF-binding protein (IGFBP) gene family. Although six IGFBPs have been identified and studied in mammals, their nonmammalian orthologs remain poorly defined. In this study, we cloned and characterized the full-length zebrafish IGFBP-1. Sequence analysis indicated that its structure is homologous to mammalian IGFBP-1. Using in situ RNA hybridization and RT-PCR, we discovered that IGFBP-1 mRNA was present in all early embryonic stages albeit at very low levels. IGFBP-1 mRNA was initially expressed in multiple embryonic tissues but became restricted to the liver shortly after hatching. In the adult stage, IGFBP-1 mRNA was found only in the liver at low levels. Prolonged food deprivation caused a significant increase in the hepatic IGFBP-1 mRNA levels, and refeeding restored the IGFBP-1 mRNA to the basal levels. When adult fish or embryos were subjected to hypoxic conditions, the IGFBP-1 mRNA expression increased dramatically. Intriguingly, the hypoxia-induced IGFBP-1 expression operated in different embryonic tissues in a developmental-stage-dependent manner. In early embryos, hypoxia-stimulated IGFBP-1 mRNA expression in the pharyngeal arches, ventricle, atrium, and brain. After hatching, the hypoxia-induced IGFBP-1 expression became liver specific. These results not only provide new information about the structural conservation, developmental expression, and physiological regulation of the IGFBP-1 gene but also present the opportunity to elucidate the developmental role of IGFBP-1 using a unique vertebrate model organism.
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