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Nucleic Acids Research, 2001, Vol. 29, No. 2 573-577
© 2001 Oxford University Press

Target DNA chromatinization modulates nicking by L1 endonuclease

Gregory J. Cost1, Amit Golding1,2, Mark S. Schlissel3 and Jef D. Boeke1,*

1Department of Molecular Biology and Genetics and 2Department of Medicine, Johns Hopkins University School of Medicine, 725 North Wolfe Street, Baltimore, MD 21205, USA and 3Department of Molecular and Cell Biology, University of California at Berkeley, Berkeley, CA 94720-3200, USA

L1 elements are human transposons which replicate via an RNA intermediate. At least 15% of the human genome is composed of L1 sequence. An important initial step in the transposition reaction is nicking of the genomic DNA by L1 endonuclease (L1 EN). In vivo much of the genome exists in the form of chromatin or is undergoing biochemical transactions such as transcription, replication or repair, which may alter the accessibility of the L1 transposition machinery to DNA. To investigate this possibility we have examined the effect of substrate chromatinization on the ability of L1 EN to nick DNA. We find that DNA incorporated into nucleosomes is generally refractory to nicking by L1 EN. Interestingly, nicking of a minority of DNA sequences is enhanced when included in chromatin. Thus, dynamic epigenetic factors such as chromatinization are likely to influence the relatively permanent placement of L1 and other retroelements in the human genome.

* To whom correspondence should be addressed. Tel: +1 410 955 0398; Fax: +1 410 614 2987; Email: jboeke{at}jhmi.edu


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