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Vol. 15, No. 24, pp. 3237-3242, December 15, 2001
Cell Biology Program, Memorial Sloan-Kettering Cancer Center, and
Cornell University Graduate School of Medical Sciences, New York, New
York 10021, USA
Chromosomal double-strand breaks (DSBs) in mammalian cells are
repaired by either homology-directed repair (HDR),
using a homologous sequence as a repair template, or nonhomologous
end-joining (NHEJ), which often involves sequence alterations at the
DSB site. To characterize the interrelationship of these two pathways,
we analyzed HDR of a DSB in cells deficient for NHEJ components. We
find that the HDR frequency is enhanced in Ku70
/,
XRCC4/, and DNA-PKcs/
cells, with the increase being particularly striking in
Ku70/ cells. Neither sister-chromatid exchange
nor gene-targeting frequencies show a dependence on these NHEJ
proteins. A Ku-modulated two-ended versus one-ended chromosome break
model is presented to explain these results.
[Key Words: Homologous recombination; DNA double-strand break; nonhomologous end-joining; Ku protein; DNA-PK; sister-chromatid exchange; gene targeting]
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