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Nucleic Acids Research, 1988, Vol. 16, No. 18 8963-8976
© 1988

Articles

Expression and amplification in transgenic mice of a polyoma virus mutant regulatory region

Bernd Krippl+, Anne E. Griep, Kathleen A. Mahon, Ernst Böhnlein§, Peter Grussø and Heiner Westphal*

Laboratory of Molecular Genetics, National Institute of Child Health and Human Development Bethesda, MD 20892, USA

*To whom correspondence should be addressed

Received April 11, 1988. Revised August 23, 1988. Accepted August 23, 1988.

Two hybrid gene constructs consisting of wild-type and mutant polyoma regulatory regions fused to a bacterial reporter gene were inserted in the mouse germline. Both transgenes were expressed in a large number of different organs. However, marker gene expression controlled by the polyoma wild-type regulatory region was not detectable in the early embryo and remained low throughout the life of the animal while expression controlled by the polyoma F9-1 mutation was detectable in blastocysts and was significantly higher at later stages of development. The F9-1 hybrid gene was also amplifiable when large T-antigen was supplied in trans to mice or to kidney cells derived from these transgenic mice. Amplification resulted in the appearance of several hundred copies of episomal transgenes and a marked increase of marker gene RNA and protein. Our results suggest that the F9-1 mutation does not alter the target spectrum of gene expression in vivo but does create a more efficient enhancer element in the polyoma early control region. Transgene amplification based upon use of the polyoma regulatory elements may be a means of increasing expression of genes in transgenic mice.

+Present address: Department of Genetics and Development, College of Physicians and Surgeons, Columbia University, New York, NY 10032

§Present address: Howard Hughes Medical Institute, Duke University Medical Center Durham, NC 27710, USA

øPresent address: Department of Molecular and Cell Biology, Max-Planck Institute of Biophysical Chemistry, D-3400 Göttingen, FRG


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