Langston Lance D, O'Donnell Mike
Howard Hughes Medical Institute, The Rockefeller University, New York City, New York 10021, USA.
Mol Cell. 2006 Jul 21;23(2):155-60. doi: 10.1016/j.molcel.2006.05.034.
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.
随着复制叉的推进，不连续滞后链的合成需要频繁地引发以及滞后链聚合酶循环至新的引物。看来这种机制还允许绕过两条链上的模板损伤，将损伤留在单链缺口处，从而防止复制叉停滞或崩溃。
