HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS		QUICK SEARCH:   [advanced] Author: Keyword(s): Year:  Vol:  Page:

J. Biol. Chem., Vol. 276, Issue 42, 39186-39191, October 19, 2001

This Article Full Text Full Text (PDF) All Versions of this Article: 276/42/39186    most recent M104411200v1 Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Smelkova, N. Articles by Marians, K. J. Search for Related Content PubMed PubMed Citation Articles by Smelkova, N. Articles by Marians, K. J.

Timely Release of Both Replication Forks from oriC Requires Modulation of Origin Topology^*

From the Molecular Biology Program, Memorial Sloan-Kettering Cancer Center, New York, New York 10021

Initiation of DNA replication at oriC occurs bidirectionally both in vivo and in vitro. Although the proteins involved in establishing the replication forks are known, little is known about the events that ensure that initiation is bidirectional. We show here that in the absence of DNA gyrase, replication fork progression from oriC on a plasmid template in vitro is unidirectional, although both replication forks have formed at the origin. There was no bias in the release of one fork or the other, ruling out protein blockage of one fork as a possible reason for the asymmetric release. Timely release of both forks required the presence of either DNA gyrase or topoisomerase IV, suggesting that modulation of the topology of the origin region is the governing factor.

N.S. dedicates this paper to the memory of Elena Smelkova.

This article has been cited by other articles:

				R. Gonzalez-Soltero, E. Botello, and A. Jimenez-Sanchez Initiation of Heat-Induced Replication Requires DnaA and the L-13-mer of oriC J. Bacteriol., December 1, 2006; 188(23): 8294 - 8298. [Abstract] [Full Text] [PDF]

				B. T. I. Payne, I. C. van Knippenberg, H. Bell, S. R. Filipe, D. J. Sherratt, and P. McGlynn Replication fork blockage by transcription factor-DNA complexes in Escherichia coli Nucleic Acids Res., October 6, 2006; 34(18): 5194 - 5202. [Abstract] [Full Text] [PDF]

				J. Thirlway, I. J. Turner, C. T. Gibson, L. Gardiner, K. Brady, S. Allen, C. J. Roberts, and P. Soultanas DnaG interacts with a linker region that joins the N- and C-domains of DnaB and induces the formation of 3-fold symmetric rings Nucleic Acids Res., June 1, 2004; 32(10): 2977 - 2986. [Abstract] [Full Text] [PDF]

				C. H. Gross, J. D. Parsons, T. H. Grossman, P. S. Charifson, S. Bellon, J. Jernee, M. Dwyer, S. P. Chambers, W. Markland, M. Botfield, et al. Active-Site Residues of Escherichia coli DNA Gyrase Required in Coupling ATP Hydrolysis to DNA Supercoiling and Amino Acid Substitutions Leading to Novobiocin Resistance Antimicrob. Agents Chemother., March 1, 2003; 47(3): 1037 - 1046. [Abstract] [Full Text] [PDF]