This Article Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Request Copyright Permission Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Goodman, H. S. Articles by Rosen, J. M. Search for Related Content PubMed PubMed Citation Articles by Goodman, H. S. Articles by Rosen, J. M.

Transcriptional Analysis of the Mouse β-Casein Gene

Department of Cell Biology, Baylor College of Medicine Houston, Texas 77030

Address requests for reprints to: Dr. Jeffrey M. Rosen, Department of Cell Biology, Baylor College of Medicine, One Baylor Plaza, Houston, Texas 77030.

Abstract

These studies were designed to further elucidate the relative contributions of transcriptional and posttranscriptional mechanisms involved in βcasein gene regulation in the mammary epithelial cell line designated COMMA-D and a clonal subline designated HC-11. Primary transcripts were mapped under various hormonal and substratum conditions using the technique of nuclear run-on transcription and single stranded sense and antisense probes spanning the β-casein gene. In the presence of insulin alone very little sense transcription is detectable, but antisense transcription is observed, which originates at least 150 basepairs upstream of the normal start site of transcription and is present regardless of hormonal, cell substratum, cell type, or gene activity. Antisense transcription is also detectable in the 3' end of the gene. Insulin, glucocorticoids, and PRL are all necessary for a maximal increase in transcription. A 2- to 4-fold increase in transcriptional activity is observed in the presence of insulin and PRL compared to insulin alone, and this is accompanied by a 125-fold increase in the level of β-casein mRNA. All three hormones act synergistically to induce a 10-fold increase in transcriptional activity, but the transcriptional increase across the gene is not equimolar. The 5β half of the gene is transcribed at a level that is 2- to 10-fold lower than that of the 3β half of the gene. These studies reveal a significant transcriptional component to β-casein gene regulation which was not heretofore detected using double stranded cDNA probes representative of only the 3' half of the gene.

FOOTNOTES

This work was supported by Grant CA-16303 from the NIH.

Received for publication July 5, 1990. Revision received August 15, 1990. Accepted for publication August 16, 1990.

This article has been cited by other articles:

				D. L. Hadsell, S. Bonnette, J. George, D. Torres, Y. Klementidis, S. Gao, P. M. Haney, J. Summy-Long, M. S. Soloff, A. F. Parlow, et al. Diminished Milk Synthesis in Upstream Stimulatory Factor 2 Null Mice Is Associated With Decreased Circulating Oxytocin and Decreased Mammary Gland Expression of Eukaryotic Initiation Factors 4E and 4G Mol. Endocrinol., November 1, 2003; 17(11): 2251 - 2267. [Abstract] [Full Text] [PDF]

				W. K. Shea-Eaton, P.-P. H. Lee, and M. M. Ip Regulation of Milk Protein Gene Expression in Normal Mammary Epithelial Cells by Tumor Necrosis Factor Endocrinology, June 1, 2001; 142(6): 2558 - 2568. [Abstract] [Full Text] [PDF]

				C. A. Myers, C. Schmidhauser, J. Mellentin-Michelotti, G. Fragoso, C. D. Roskelley, G. Casperson, R. Mossi, P. Pujuguet, G. Hager, and M. J. Bissell Characterization of BCE-1, a Transcriptional Enhancer Regulated by Prolactin and Extracellular Matrix and Modulated by the State of Histone Acetylation Mol. Cell. Biol., April 1, 1998; 18(4): 2184 - 2195. [Abstract] [Full Text]