Hu, X., Bulger, M., Roach, J. N., Eszterhas, S. K., Olivier, E., Bouhassira, E. E., Groudine, M. T. and Fiering, S. (2003) Promoters of the murine embryonic beta-like globin genes Ey and betah1 do not compete for interaction with the beta-globin locus control region. Proceedings of the National Academy of Sciences of the United States of America, 100(3), pp. 1111-1115. (doi: 10.1073/pnas.0337404100)
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Publisher's URL: http://dx.doi.org/10.1073/pnas.0337404100
Abstract
Mammalian β-globin loci contain multiple β-like genes that are expressed at different times during development. The murine β-globin locus contains two genes expressed during the embryo stage, Ey and βh1, and two genes expressed at both the fetal and postnatal stages, β-major and β-minor. Studies of transgenic human β-like globin loci in mice have suggested that expression of one gene at the locus will suppress expression of other genes at the locus. To test this hypothesis we produced mouse lines with deletions of either the Ey or βh1 promoter in the endogenous murine β-globin locus. Promoter deletion eliminated expression of the mutant gene but did not affect expression of the remaining embryonic gene or the fetal/adult β-globin genes on the mutant allele. These results demonstrate a lack of competitive effects between individual mouse embryonic β-globin gene promoters and other genes in the locus. The implication of these findings for models of β-globin gene expression are discussed.
| Item Type: | Articles |
|---|---|
| Status: | Published |
| Refereed: | Yes |
| Glasgow Author(s) Enlighten ID: | Olivier, Dr Emmanuel |
| Authors: | Hu, X., Bulger, M., Roach, J. N., Eszterhas, S. K., Olivier, E., Bouhassira, E. E., Groudine, M. T., and Fiering, S. |
| College/School: | College of Medical Veterinary and Life Sciences > School of Cardiovascular & Metabolic Health |
| Journal Name: | Proceedings of the National Academy of Sciences of the United States of America |
| Publisher: | National Academy of Sciences |
| ISSN: | 0027-8424 |
| ISSN (Online): | 1091-6490 |
| Related URLs: |
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