Expression of a secretory protein gene during androgen-induced cell growth

J. T. Moore, M. E. Norvitch, E. D. Wieben, C. M. Veneziale

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12 Scopus citations


Guinea pig seminal vesicle epithelium is an androgen-dependent tissue composed of tall columnar cells which synthesize four major secretory proteins designated SVP-1-4. Castration promptly causes the seminal vesicle epithelium cells to undergo major morphological changes. By the fifth day after castration, cell number decreases to 12% of normal, and the surviving cells are greatly involuted structurally. An injection of testosterone was sufficient to stimulate individual cell growth to the normal tall columnar configuration by 48 h without increasing cell number. Cell growth following testosterone was preceded by a 4-fold increase between 0-12 h in total cellular RNA signifying a large increase in rRNAs. To aid in the analysis of gene expression during androgen repletion, we identified a cDNA plasmid clone representing the 3'-end of the mRNA of SVP-4. The clone pAT 76 was identified by hybrid-select translation and characterization of the product of in vitro translation. The steady-state levels of SVP-4 mRNA in blots of total cellular RNA increased between 0-24 h; this appeared to be due mainly to a general nonselective increase in all or most of the abundant mRNAs. We demonstrated by in vitro translation studies that the corresponding transcript was still present during the 5th and 36th days of castration without having undergone a selective loss in abundance and during hormone repletion without undergoing a selective increase. Testosterone exerted an early and more conspicuous effect on rRNA synthesis. Whether direct or indirect this may be a key event underlying the ultimate action of testosterone, namely maintenance of cell structure.

Original languageEnglish (US)
Pages (from-to)14750-14756
Number of pages7
JournalJournal of Biological Chemistry
Issue number23
StatePublished - 1984

ASJC Scopus subject areas

  • Biochemistry
  • Molecular Biology
  • Cell Biology


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