Identification of estrogen-responsive genes in the testis of sea bream (Sparus auratus) using suppression subtractive hybridization. | - CCMAR -

Journal Article

TitleIdentification of estrogen-responsive genes in the testis of sea bream (Sparus auratus) using suppression subtractive hybridization.
Publication TypeJournal Article
AuthorsPinto, PIS, Teodósio, R, Galay-Burgos, M, Power, DM, Sweeney, GE, Canario, AVM
Year of Publication2006
JournalMol Reprod Dev
Volume73
Issue3
Date Published2006 Mar
Pagination318-29
ISSN1040-452X
KeywordsAnimals, Apolipoprotein A-I, Cloning, Molecular, Dose-Response Relationship, Drug, Down-Regulation, Estradiol, Estrogens, Fibrinogen, Gene Expression Profiling, Liver, Male, Nucleic Acid Hybridization, Reverse Transcriptase Polymerase Chain Reaction, Sea Bream, Testis, Up-Regulation, Vitellogenins
Abstract

There is growing evidence that estrogens play important roles in both normal and xenoestrogen disrupted testis physiology. However, the mechanisms and signaling pathways involved, in particular in fish, are largely unknown. We have used suppression subtractive hybridization to isolate 152 candidate estrogen-responsive genes in the testis of male estradiol (E2)-treated sea bream (Sparus aurata). The E2 up-regulation of some of the genes (e.g., choriogenin L and H, vitellogenin I and II, apolipoprotein A-I, fibrinogen beta and gamma, and thyroid receptor interacting protein 4) was confirmed by reverse transcriptase polymerase chain reaction in fish treated with 0.1-10 mg/kg E2. Many of these genes are typical E2-induced genes in liver, and this is the first report of its up regulation with E2 in testis. Moreover, low levels of expression were also found for nontreated fish. Hepatic differential expression for these genes was also confirmed, although, contrary to testis, fibrinogen beta, and gamma were downregulated. The possible significance of these findings in normal testis physiology and in endocrine disruption is discussed.

DOI10.1002/mrd.20402
Sapientia

http://www.ncbi.nlm.nih.gov/pubmed/16267841?dopt=Abstract

Alternate JournalMol. Reprod. Dev.
PubMed ID16267841