This Article Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Services Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Reprints and Permissions Copyright Information Books from ASM Press MicrobeWorld Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by MacKenzie, K L Articles by Symonds, G Search for Related Content PubMed PubMed Citation Articles by MacKenzie, K L Articles by Symonds, G

 Previous Article  |  Next Article 

J Virol. 1994 November; 68(11): 6924-6932

An internal deletion enhances the transcriptional activity of a recombinant retrovirus in hematopoietic cells in vivo.

Children's Medical Research Institute, Wentworthville, New South Wales, Australia.

ABSTRACT

Lv-myc is a recombinant retrovirus that spontaneously arose during experiments designed to express the provirus LNAv-myc in the hematopoietic system of bone marrow-reconstituted mice (L. Bonham, K. MacKenzie, S. Wood, P. B. Rowe, and G. Symonds, Oncogene 7:2219-2229, 1992). The recombinant provirus is of interest because it is able to promote long terminal repeat-initiated transcription in hematopoietic cells in vivo, whereas the parental provirus, LNAv-myc, is transcriptionally repressed in the same cells. Here we report that Lv-myc was generated by precise deletion of the neomycin resistance gene (neo) and the human gamma-actin promoter from LNAv-myc. In comparison with LNAv-myc, no sequence alterations in the viral regulatory regions of Lv-myc were detected. Thus, it appears that neo and/or the gamma-actin promoter exerted a cis-acting repressor effect on the long terminal repeat of LNAv-myc in vivo. The origin of Lv-myc was also investigated, and it was shown that Lv-myc was harbored as a productive provirus in a G418-resistant subpopulation of the LNAv-myc producer cell line, psi 2AV. It appears that Lv-myc arose during propagation of the psi 2AV cell line. Repeated sequence detected at the sites of the deletion suggest that Lv-myc was generated by a template misalignment during reverse transcription of LNAv-myc.

This article has been cited by other articles:

• MacKenzie, K.L., Dolnikov, A., Millington, M., Shounan, Y., Symonds, G. (1999). Mutant N-ras Induces Myeloproliferative Disorders and Apoptosis in Bone Marrow Repopulated Mice. Blood 93: 2043-2056 [Abstract] [Full Text]