Insulin-like growth factor-I of pejerrey, Odontesthes bonariensis: cDNA characterization, tissue distribution and expression profiles after growth hormone administration
✍ Scribed by Andrés A. Sciara; Gustavo. M. Somoza; Silvia. E. Arranz
- Publisher
- Wiley (John Wiley & Sons)
- Year
- 2008
- Tongue
- English
- Weight
- 416 KB
- Volume
- 309A
- Category
- Article
- ISSN
- 1932-5223
- DOI
- 10.1002/jez.466
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✦ Synopsis
Abstract
The liver production of the insulin‐like growth factor‐I (IGF‐I) is a key factor in the endocrine control of body growth by a growth hormone. As pejerrey Odontesthes bonariensis has been reported as a fish with low growth rates in captivity, basic research on this respect is needed in order to understand it. In this context, the pejerrey IGF‐I cDNA was cloned and its hepatic expression was examined in fish after recombinant pejerrey growth hormone (pjGHr) administration. The full length of IGF‐I transcript showed a high sequence similarity to other teleost sequences. The tissue distribution analysis by reverse transcriptase polymerase chain reaction in adult fish revealed that IGF‐I expressed ubiquitously with the highest mRNA levels in the liver, posterior intestine and brain. No alternative IGF‐I mRNA was found in the liver, as it was reported for other teleosts. IGF‐I transcript was measured in the liver after pjGHr in vivo stimulation by means of quantitative real‐time polymerase chain reaction assays. A dose‐dependent response of IGF‐I mRNA was observed after pjGHr administration, and reached a six‐fold IGF‐I maximum increase over control group when 2.5 µg pjGH/g‐body weight (bw) was injected. Temporal analysis of hepatic IGF‐I mRNA level showed that administration of a single dose of pjGHr into juvenile pejerrey resulted in a significant increase (P<0.02) 9 hours post‐injection (hpi). These results add novel information on the nucleotide sequence of IGF‐I in Atheriniformes and demonstrate that pjGHr could promote a dramatic response in liver, increasing the IGF‐I mRNA level. J. Exp. Zool. 309A:407–418, 2008. © 2008 Wiley‐Liss, Inc.