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Repression of the inhibin alpha-subunit gene by the transcription factor CCAAT/enhancer-binding protein-beta

  1. Author:
    Burkart, A. D.
    Mukherjee, A.
    Sterneck, E.
    Johnson, P. F.
    Mayo, K. E.

  2. Author Address

    Northwestern Univ, Dept Biochem Mol Biol & Cell Biol, Evanston, IL 60208 USA. Northwestern Univ, Ctr Reprod Sci, Evanston, IL 60208 USA. Harvard Univ, Sch Med, Massachusetts Gen Hosp, Boston, MA 02114 USA. NCI, Mol Mech Dev Grp, Lab Prot Dynam & Signaling, Ctr Canc Res, Frederick, MD 21702 USA. NCI, Eukaryot Transcript Regulat Sect, Lab Prot Dynam & Signaling, Frederick, MD 21702 USA Mayo, KE, Northwestern Univ, Dept Biochem Mol Biol & Cell Biol, 2153 Sheridan Rd, Evanston, IL 60208 USA
    1. Year: 2005
    2. Date: APR
  2. Journal: Endocrinology
    1. 146
    2. 4
    3. Pages: 1909-1921
  4. Type of Article: Article
  1. Abstract:

    Inhibin is a dimeric peptide hormone produced in ovarian granulosa cells that suppresses FSH synthesis and secretion in the pituitary. Expression of inhibin alpha- and beta- subunit genes in the rodent ovary is positively regulated by FSH and negatively regulated after the preovulatory LH surge. We have investigated the role of the transcription factor CCAAT/ enhancer- binding protein- beta ( C/ EBP beta) in repressing the inhibin alpha- subunit gene. C/ EBP beta knockout mice fail to appropriately down- regulate inhibin alpha- subunit mRNA levels after treatment with human chorionic gonadotropin, indicating that C/ EBP beta may function to repress inhibin gene expression. The expression and regulation of C/ EBP beta were examined in rodent ovary, and these studies show that C/ EBP beta is expressed in ovary and granulosa cells and is induced in response to human chorionic gonadotropin. Transient cotransfections with an inhibin promoter- luciferase reporter in a mouse granulosa cell line, GRMO2 cells, show that C/ EBP beta is capable of repressing both basal and forskolin- stimulated inhibin gene promoter activities. An upstream binding site for C/ EBP beta in the inhibin alpha- subunit promoter was identified by electrophoretic mobility shift assays, which, when mutated, results in elevated inhibin promoter activity. However, C/ EBP beta also represses shorter promoter constructs lacking this site, and this component of repression is dependent on the more proximal promoter cAMP response element ( CRE). Electrophoretic mobility shift assays show that C/ EBP beta effectively competes with CRE- binding protein for binding to this atypical CRE. Thus, there are two distinct mechanisms by which C/ EBP beta represses inhibin alpha- subunit gene expression in ovarian granulosa cells

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  1. View record in Web of Science®
  2. WOS: 000227667400031

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