Glucocorticoid hormone-dependent maturation of the mouse mammary tumor virus (MMTV) Glucocorticoid hormones elicit many types of responses in a variety of target tissues and in vitro-cultured cell lines (1, 4, 24; K. R. Yamamoto, Annu. Rev. Genet., in press). These hormonal effects appear to be mediated by specific intracellular receptor proteins; the steroid-receptor interaction potentiates a functional change in the receptor that results in its increased DNA-binding activity and selective recognition of enhancer-like sites at or around genes under glucocorticoid control (1,7,10,18,26,(31)(32)(33)(34)(35)(36)(37)44,52; Yamamoto, in press). As a result of this apparent sequence specificity for glucocorticoid-receptor complexes, the rate of transcription of glucocorticoid-regulated genes is selectively modulated and accounts for gene expression changes of certain steroid responses (1; Yamamoto, in press). However, the mechanisms of most glucocorticoid responses are unknown, and many responses may result from secondary or regulatory steroid effects in which functional gene products under direct transcriptional control affect the expression of other biologically active genes at posttranscriptional or posttranslational levels. For example, the accumulation of alpha,-acid glycoprotein mRNA appears to result from selective message stabilization after glucocorticoid treatment (50), while steroid-mediated changes in the levels or activities of specific processing enzymes have also been reported (12, 27, 45); mechanisms of these regulated processes are largely unknown. We have been using the expression and subsequent maturation of mouse mammary tumor virus (MMTV) precursor polyproteins in virally infected cell lines as versatile and sensitive probes to explore posttranslational regulatory circuits under steroid control (16,17 (17).To begin to assess the molecular details and cellular requirements of the steroid-regulated posttranslational path-574 on May 10, 2018 by guest