JB
Home Help [Feedback] [For Subscribers] [Archive] [Search] [Contents]
This Article
Right arrow Full Text
Right arrow Full Text (PDF)
Right arrow Other Versions of this Article:
JB.00814-06v1
188/23/8294    most recent
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrowReprints and Permissions
Right arrow Copyright Information
Right arrow Books from ASM Press
Right arrow MicrobeWorld
Citing Articles
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by González-Soltero, R.
Right arrow Articles by Jiménez-Sánchez, A.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by González-Soltero, R.
Right arrow Articles by Jiménez-Sánchez, A.

 Previous Article  |  Next Article 

Journal of Bacteriology, December 2006, p. 8294-8298, Vol. 188, No. 23
0021-9193/06/$08.00+0     doi:10.1128/JB.00814-06
Copyright © 2006, American Society for Microbiology. All Rights Reserved.

Initiation of Heat-Induced Replication Requires DnaA and the L-13-mer of oriC{triangledown}

Rocío González-Soltero, Emilia Botello, and Alfonso Jiménez-Sánchez*

Department of Biochemistry, Molecular Biology and Genetics, University of Extremadura, E06080-Badajoz, Spain

Received 8 June 2006/ Accepted 8 September 2006

An upshift of 10°C or more in the growth temperature of an Escherichia coli culture causes induction of extra rounds of chromosome replication. This stress replication initiates at oriC but has functional requirements different from those of cyclic replication. We named this phenomenon heat-induced replication (HIR). Analysis of HIR in bacterial strains that had complete or partial oriC deletions and were suppressed by F integration showed that no sequence outside oriC is used for HIR. Analysis of a number of oriC mutants showed that deletion of the L-13-mer, which makes oriC inactive for cyclic replication, was the only mutation studied that inactivated HIR. The requirement for this sequence was strictly correlated with Benham's theoretical stress-induced DNA duplex destabilization. oriC mutations at DnaA, FIS, or IHF binding sites showed normal HIR activation, but DnaA was required for HIR. We suggest that strand opening for HIR initiation occurs due to heat-induced destabilization of the L-13-mer, and the stable oligomeric DnaA-single-stranded oriC complex might be required only to load the replicative helicase DnaB.

* Corresponding author. Mailing address: Department of Biochemistry, Molecular Biology and Genetics, University of Extremadura, E06080-Badajoz, Spain. Phone: 34-924-289421. Fax: 34-924-273260. E-mail: a.jimenezsanchez{at}gmail.com.

{triangledown} Published ahead of print on 15 September 2006.

Journal of Bacteriology, December 2006, p. 8294-8298, Vol. 188, No. 23
0021-9193/06/$08.00+0     doi:10.1128/JB.00814-06
Copyright © 2006, American Society for Microbiology. All Rights Reserved.





Home Help [Feedback] [For Subscribers] [Archive] [Search] [Contents]
Appl. Environ. Microbiol. Infect. Immun. Eukaryot. Cell
Mol. Cell. Biol. J. Virol. Microbiol. Mol. Biol. Rev.
ALL ASM JOURNALS

Copyright © 2006 by the American Society for Microbiology. All rights reserved.