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Journal of Molecular Endocrinology (1992) 8, 193-201    DOI: 10.1677/jme.0.0080193
© 1992 Society for Endocrinology

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The expression of a putative insulin-like growth factor-I receptor gene in the liver of the developing chick

D. G. Armstrong and C. O. Hogg

The biological activity of insulin-like growth factor-I (IGF-I) is mediated by a transmembrane glycoprotein (type-1 IGF receptor or IGF-I receptor) that shows considerable sequence homology with the insulin receptor. In order to detect the expression of this gene in chicken liver tissue, a plasmid was constructed containing a fragment of chicken IGF-I receptor cDNA. The cDNA fragment corresponded to nucleotides 326–599 of the human IGF-I receptor cDNA and showed 86.1 and 69.3% homology at the nucleotide level and 96.7 and 80.2% homology at the amino acid level with the human IGF-I receptor and insulin receptor respectively. The construct was used to generate an antisense RNA probe for the detection of IGF-I receptor mRNA transcripts in 1- and 4-week-old chick liver tissue.

IGF-I receptor gene expression was initially detected by the reverse transcriptase polymerase chain reaction using synthetic chicken IGF-I receptor oligonucleotides. Amplified fragments of the correct size were detected in both RNA samples. Northern blots were also used to detect IGF-I receptor mRNA transcripts in the liver RNA samples. The results indicated that the amount of receptor mRNA decreased significantly between 1 and 4 weeks after hatch. In contrast, chicken β-actin gene expression remained constant over this period. A major IGF-I receptor RNA transcript (11 kb) was observed in blots from 1-week-old livers, less abundant transcripts were also observed ranging in size from 8 to 9 kb. No bands were detected in blots from 4-week-old livers.

The results indicate that the steady-state level of chicken liver IGF-I receptor mRNA decreased significantly 1–4 weeks after hatch. It is not known whether this difference was due to a decrease in gene expression and/or an increase in the rate of IGF-I receptor mRNA degradation.







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