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Nucleic Acids Research, 1990, Vol. 18, No. 8 2069-2077
© 1990

MOLECULAR BIOLOGY

Independent regulation of mouse VL30 retrotransposon expression in response to serum and oncogenic cell transformation

Lynne Eaton and John D. Norton*

Department of Haematology, Royal Free Hospital School of Medicine Pond Street, London NW3 2QG, UK

* To whom correspondence should be addressed

Received December 20, 1989. Revised March 26, 1990. Accepted March 26, 1990.

The nucleotide sequence of the long terminal repeats (LTRs) of retrovirus-transmissible mouse VL30 cDNA clones, NVL-1 and NVL-2 were determined and compared with that of the prototype NVL-3. Both shared the typical U3 R U5 structure together with unusual features of redundancy in the tRNAgty primer binding site and adjacent inverted repeat. NVL-1 and NVL-2 LTRs were almost identical and differed from the NVL-3 LTR in the U3 domain harbouring transcriptional regulatory determinants. S1 nuclease analysis of cellular and virus-encapsidated RNA suggested that NVL-1/2 and NVL-3 elements retrotranspose with comparable efficiency but that in contrast to transformation-regulated VL30 expression which affects all types of NVL element, only NVL-1/2 elements were found to be serum responsive. Both modes of VL30 regulation were found to be coupled through protein kinase C-independent pathways. Expression of N-ras transactivated U3 enhancer determinants in all classes of LTR. However the same region of NVL-1/2 LTR did not confer serum responsiveness implying that cis regulatory determinants of VL30 elements mediating growth factor responsiveness are at least in part dissociable from those responsible for cell transformation-regulated expression.


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