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Human Molecular Genetics, 2001, Vol. 10, No. 22 2481-2491
© 2001 Oxford University Press

Mechanisms of MLL gene rearrangement: site-specific DNA cleavage within the breakpoint cluster region is independent of chromosomal context

Martin Stanulla2,4, Pradheepkumar Chhalliyil2, Junjie Wang2, Sheila N. Jani-Sait3 and Peter D. Aplan1,+

1Genetics Branch, Center for Cancer Research, National Cancer Institute, Gaithersburg, MD, USA, 2Department of Cancer Genetics and 3Department of Clinical Cytogenetics, Roswell Park Cancer Institute, USA and 4Department of Pediatric Hematology and Oncology, Hannover Medical School, Hannover, Germany

The MLL gene at chromosome band 11q23 is specifically cleaved at a unique site within its breakpoint cluster region (bcr) during the higher order chromatin fragmentation associated with apoptosis. We now show that the same specific DNA cleavage event can be detected in an exogenous MLL bcr fragment that is integrated into the genome outside of its normal chromosomal context, as well as in an extrachromosomal episome containing an MLL bcr fragment. We also show that episomal or randomly integrated copies of the MLL bcr behave similar to the endogenous MLL bcr when tested in a scaffold-associated region (SAR) assay. Furthermore, an episomal murine MLL bcr introduced into human cells is cleaved at the same site as the endogenous murine MLL bcr; this episomal murine MLL bcr also functions as a SAR in human cells. We conclude that both nuclear DNA scaffold attachment as well as site-specific DNA cleavage can be directed by sequences contained within the MLL bcr, and that it is feasible to study these events using episomal shuttle vectors.

+ To whom correspondence should be addressed at: National Cancer Institute, Advanced Technology Center, 8717 Grovemont Circle, Gaithersburg, MD 20877, USA. Tel: +1 301 435 5005; Fax: +1 301 402 3134; Email: aplanp@mail.nih.gov


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