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Mol Cell Biol, August 1998, p. 4433-4443, Vol. 18, No. 8
0270-7306/98/$04.00+0
Copyright © 1998, American Society for Microbiology. All rights reserved.

An Alternative Promoter in the Mouse Major Histocompatibility Complex Class II I-Abeta Gene: Implications for the Origin of CpG Islands

Donald Macleod,1 * Robin R. Ali,2 and Adrian Bird1

Institute of Cell and Molecular Biology, University of Edinburgh, Edinburgh EH9 3JR, Scotland,1 and Department of Molecular Genetics, Institute of Ophthalmology, London ECIV 9EL, United Kingdom2

Received 29 December 1997/Returned for modification 6 March 1998/Accepted 19 May 1998

Nonmethylated CpG islands are generally located at the 5' ends of genes, but a CpG island in the mouse major histocompatibility complex class II I-Abeta gene is remote from the promoter and covers exon 2. We have found that this CpG island includes a novel intronic promoter that is active in embryonic and germ cells. The resulting transcript potentially encodes a severely truncated protein which would lack the signal peptide and external beta 1 domains. The functional significance of the internal CpG island may be to facilitate gene conversion, thereby sustaining the high level of polymorphism seen at exon 2. Deletions of the I-Abeta CpG island promoter reduce transcription and frequently lead to methylation of the CpG island in a transgenic mouse assay. These and other results support the idea that all CpG islands arise at promoters that are active in early embryonic cells.

* Corresponding author. Mailing address: Institute of Cell and Molecular Biology, The University of Edinburgh, Darwin Building, King's Buildings, Mayfield Road, Edinburgh EH9 3JR, Scotland. Phone: 0131 650 5819. Fax: 0131 650 5379. E-mail: Donald.Macleod{at}ed.ac.uk.

Mol Cell Biol, August 1998, p. 4433-4443, Vol. 18, No. 8
0270-7306/98/$04.00+0
Copyright © 1998, American Society for Microbiology. All rights reserved.


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