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Submitted on December 16, 2003
Accepted on March 31, 2004
-Casein mRNA Translation by Cytoplasmic Polyadenylation
Department of Biochemistry and Molecular Biology, Louisiana State University Health Sciences Center, Shreveport, Louisiana, 71130-3932, USA, and Institute of Animal Science, The Volcani Center, Bet-Degan, Israel
* To whom correspondence should be addressed. E-mail: rrhoad{at}lsuhsc.edu.
Previous studies have shown that the synthesis and stability of milk protein mRNAs are regulated by lactogenic hormones. We demonstrate here in cultured mouse mammary epithelial cells (CID 9) that insulin plus prolactin also synergistically increase the rate of milk protein mRNA translation. Insulin alone stimulates synthesis of both milk and non-milk proteins, while prolactin alone has no effect, but insulin plus prolactin selectively stimulates synthesis of milk proteins more than insulin alone. The increase in 
-casein mRNA translation is also reflected in a shift to larger polysomes, indicating an effect on translational inititation. Inhibitors of the PI3K, mTOR, and MAPK pathways block insulin-stimulated total protein and -casein synthesis but not the synergistic stimulation. Conversely, cordycepin abolishes synergistic stimulation of protein synthesis without affecting insulin-stimulated translation. The poly(A) tract of -casein mRNA progressively increases from 
20 to 200 A residues over 30 min of treatment with insulin plus prolactin. The 3'-untranslated region of -casein mRNA containing an unaltered CPE is sufficient for the translational enhancement and mRNA-specific polyadenylation, based on transient transfection of cells with a reporter construct. Insulin and prolactin stimulate CPEB phosphorylation with no increase of cytoplasmic poly(A) polymerase activity.
-casein mRNA •
cytoplasmic polyadenylation •
mouse mammary epithelial cells •
mRNA-specific translational control •
synergistic hormone action
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