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Journal of Bacteriology, September 2008, p. 5870-5878, Vol. 190, No. 17
0021-9193/08/$08.00+0     doi:10.1128/JB.00479-08
Copyright © 2008, American Society for Microbiology. All Rights Reserved.

Excess SeqA Leads to Replication Arrest and a Cell Division Defect in Vibrio cholerae{triangledown}

Djenann Saint-Dic,1 Jason Kehrl,1 Brian Frushour,1 and Lyn Sue Kahng1,2*

Section of Digestive Diseases and Nutrition, University of Illinois at Chicago,1 Jesse Brown VA Medical Center, University of Illinois at Chicago, Chicago, Illinois 606122

Received 8 April 2008/ Accepted 30 June 2008

Although most bacteria contain a single circular chromosome, some have complex genomes, and all Vibrio species studied so far contain both a large and a small chromosome. In recent years, the divided genome of Vibrio cholerae has proven to be an interesting model system with both parallels to and novel features compared with the genome of Escherichia coli. While factors influencing the replication and segregation of both chromosomes have begun to be elucidated, much remains to be learned about the maintenance of this genome and of complex bacterial genomes generally. An important aspect of replicating any genome is the correct timing of initiation, without which organisms risk aneuploidy. During DNA replication in E. coli, newly replicated origins cannot immediately reinitiate because they undergo sequestration by the SeqA protein, which binds hemimethylated origin DNA. This DNA is already methylated by Dam on the template strand and later becomes fully methylated; aberrant amounts of Dam or the deletion of seqA leads to asynchronous replication. In our study, hemimethylated DNA was detected at both origins of V. cholerae, suggesting that these origins are also subject to sequestration. The overproduction of SeqA led to a loss of viability, the condensation of DNA, and a filamentous morphology. Cells with abnormal DNA content arose in the population, and replication was inhibited as determined by a reduced ratio of origin to terminus DNA in SeqA-overexpressing cells. Thus, excessive SeqA negatively affects replication in V. cholerae and prevents correct progression to downstream cell cycle events such as segregation and cell division.

* Corresponding author. Mailing address: Section of Digestive Diseases and Nutrition, Jesse Brown VA Medical Center, University of Illinois at Chicago, 840 S. Wood St., M/C 716, Chicago, IL 60612. Phone: (312) 996-6387. Fax: (312) 996-5103. E-mail: lynsue{at}uic.edu

{triangledown} Published ahead of print on 11 July 2008.

Journal of Bacteriology, September 2008, p. 5870-5878, Vol. 190, No. 17
0021-9193/08/$08.00+0     doi:10.1128/JB.00479-08
Copyright © 2008, American Society for Microbiology. All Rights Reserved.



This article has been cited by other articles:

  • Chung, Y. S., Brendler, T., Austin, S., Guarne, A. (2009). Structural insights into the cooperative binding of SeqA to a tandem GATC repeat. Nucleic Acids Res 37: 3143-3152 [Abstract] [Full Text]  


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