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

690 Scopus citations

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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