Journal
MOLECULAR CELL
Volume 23, Issue 2, Pages 155-160Publisher
CELL PRESS
DOI: 10.1016/j.molcel.2006.05.034
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As the replication fork progresses, synthesis of the discontinuous lagging strand requires frequent priming and cycling of the lagging strand polymerase to the new primers. It appears that this mechanism also permits bypass of template lesions on both strands, leaving the damage behind in a single-strand gap and precluding fork stalling or collapse.
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