Role of progesterone and glucocorticoids in the transcription of the beta-casein and 28-S ribosomal genes in the rabbit mammary gland.

Isolated mammary nuclei were incubated in the presence of HgCTP and the neosynthesized RNA was isolated with a SH-Sepharose column. The concentration of beta-casein mRNA and 28-S ribosomal RNA in the neosynthesized RNA fractions was measured using [3H]cDNA probes complementary to beta-casein mRNA and 28-S rRNA respectively. Prolactin injected into pseudopregnant animals accelerates the transcription of both genes and increases the stability of the beta-casein mRNA but not of the 28-S rRNA. Progesterone injected simultaneously with prolactin reduced considerably all these effects of prolactin, with a lower efficiency when the highest doses of prolactin were injected. These observations suggest that progesterone attenuates the transfer of prolactin information related to the lactogenesis into the mammary cell. Glucocorticoids injected with prolactin amplify the prolactin action on the expression of the beta-casein gene but not of the 28-S rRNA genes. In the absence of prolactin (a situation obtained by injecting simultaneously CB 154, a drug which inhibits pituitary prolactin secretion) glucocorticoids exhibit no effect. In the lactating rabbit glucocorticoids do not delay significantly the drop of beta-casein gene transcription rate provoked by weaning or by prolactin withdrawal obtained by injecting CB 154. A comparison of the beta-casein mRNA accumulation and the transcription rate of the beta-casein gene indicates that glucocorticoids act essentially by amplifying the activation of beta-casein transcription supported by prolactin, but not by enhancing the stability of the beta-casein mRNA.