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• W2132088647 endingPage "1756" @default.
• W2132088647 startingPage "1747" @default.
• W2132088647 abstract "Abstract Two models have been proposed for triggering release of the lagging strand polymerase at the replication fork, enabling cycling to the primer for the next Okazaki fragment—either collision with the 5′-end of the preceding fragment (collision model) or synthesis of a new primer by primase (signaling model). Specific perturbation of lagging strand elongation on minicircles with a highly asymmetric G:C distribution with ddGTP or dGDPNP yielded results that confirmed the signaling model and ruled out the collision model. We demonstrated that the presence of a primer, not primase per se, provides the signal that triggers cycling. Lagging strand synthesis proceeds much faster than leading strand synthesis, explaining why gaps between Okazaki fragments are not found under physiological conditions." @default.
• W2132088647 created "2016-06-24" @default.
• W2132088647 creator A5005151768 @default.
• W2132088647 creator A5050914365 @default.
• W2132088647 date "2013-11-13" @default.
• W2132088647 modified "2023-09-25" @default.
• W2132088647 title "Cycling of the <i>E. coli</i> lagging strand polymerase is triggered exclusively by the availability of a new primer at the replication fork" @default.
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• W2132088647 doi "https://doi.org/10.1093/nar/gkt1098" @default.
• W2132088647 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/3919610" @default.
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• W2132088647 hasPublicationYear "2013" @default.
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