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Journal of Virology, November 2005, p. 13865-13874, Vol. 79, No. 22
0022-538X/05/$08.00+0     doi:10.1128/JVI.79.22.13865-13874.2005
Copyright © 2005, American Society for Microbiology. All Rights Reserved.

Transcriptional Regulation of Early Transposon Elements, an Active Family of Mouse Long Terminal Repeat Retrotransposons{dagger}

Irina A. Maksakova and Dixie L. Mager*

Terry Fox Laboratory, British Columbia Cancer Research Centre, 675 West 10th Avenue, Vancouver, British Columbia, V5Z 1L3, and Department of Medical Genetics, University of British Columbia, Vancouver, British Columbia, Canada

Received 12 April 2005/ Accepted 17 August 2005

While early transposon (ETn) endogenous retrovirus (ERV)-like elements are known to be active insertional mutagens in the mouse, little is known about their transcriptional regulation. ETns are transcribed during early mouse embryogenesis in embryonic stem (ES) and embryonic carcinoma (EC) cell lines. Despite their lack of coding potential, some ETns remain transposition competent through their use of reverse transcriptase encoded by a related group of ERVs—MusD elements. In this study, we have confirmed high expression levels of ETn and MusD elements in ES and EC cells and have demonstrated an increase in the copy number of ETnII elements in the EC P19 cell line. Using transient transfections, we have shown that ETnII and MusD LTRs are much more active as promoters in P19 cells than in NIH 3T3 cells, indicating that genomic context and methylation are not the only factors determining endogenous transcriptional activity of ETns. Three sites in the 5' part of the long terminal repeat (LTR) were demonstrated to bind Sp1 and Sp3 transcription factors and were found to be important for high LTR promoter activity in P19 cells, suggesting that as yet unidentified Sp binding partners are involved in the regulation of ETn activity in undifferentiated cells. Finally, we found multiple transcription start sites within the ETn LTR and have shown that the LTR retains significant promoter activity in the absence of its noncanonical TATA box. These findings lend insight into the transcriptional regulation of this family of mobile mouse retrotransposons.

* Corresponding author. Mailing address: Terry Fox Laboratory, British Columbia Cancer Research Centre, 675 West 10th Avenue, Vancouver, British Columbia V5Z 1L3, Canada. Phone: (604) 675-8139. Fax: (604) 877-0712. E-mail: dmager{at}bccrc.ca.

{dagger} Supplemental material for this article may be found at http://jvi.asm.org/.

Journal of Virology, November 2005, p. 13865-13874, Vol. 79, No. 22
0022-538X/05/$08.00+0     doi:10.1128/JVI.79.22.13865-13874.2005
Copyright © 2005, American Society for Microbiology. All Rights Reserved.



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