High frequency retrotransposition in cultured mammalian cells

John V. Moran, Susan E. Holmes, Thierry P. Naas, Ralph J. DeBerardinis, Jef D. Boeke, Haig H. Kazazian

    Research output: Contribution to journalArticle

    Abstract

    We previously isolated two human L1 elements (L1.2 and LRE2) as the progenitors of disease-producing insertions. Here, we show these elements can actively retrotranspose in cultured mammalian cells. When stably expressed from an episome in HeLa cells, both elements retrotransposed into a variety of chromosomal locations at a high frequency. The retrotransposed products resembled endogenous L1 insertions, since they were variably 5' truncated, ended in poly(A) tracts, and were flanked by target-site duplications or short deletions. Point mutations in conserved domains of the L1.2-encoded proteins reduced retrotransposition by 100- to 1000-fold. Remarkably, L1.2 also retrotransposed in a mouse cell line, suggesting a potential role for L1-based vectors in random insertional mutagenesis.

    Original languageEnglish (US)
    Pages (from-to)917-927
    Number of pages11
    JournalCell
    Volume87
    Issue number5
    DOIs
    StatePublished - Nov 29 1996

    ASJC Scopus subject areas

    • Biochemistry, Genetics and Molecular Biology(all)

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  • Cite this

    Moran, J. V., Holmes, S. E., Naas, T. P., DeBerardinis, R. J., Boeke, J. D., & Kazazian, H. H. (1996). High frequency retrotransposition in cultured mammalian cells. Cell, 87(5), 917-927. https://doi.org/10.1016/S0092-8674(00)81998-4