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Nucleic Acids Research Advance Access published online on March 20, 2009
Nucleic Acids Research, doi:10.1093/nar/gkp151
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© 2009 The Author(s)
This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/2.0/uk/) which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.

Structural Biology

Structural insights into the cooperative binding of SeqA to a tandem GATC repeat

Yu Seon Chung1, Therese Brendler2, Stuart Austin2 and Alba Guarné1,*

1Department of Biochemistry and Biomedical Sciences, Health Sciences Center, McMaster University, 1200 Main Street West, Hamilton, ON L8N 3Z5, Canada and 2Gene Regulation and Chromosome Biology Laboratory, Division of Basic Sciences, NCI-Center for Cancer Research, National Cancer Institute at Frederick, MD 21702, USA

*To whom correspondence should be addressed. Tel: +1 905 5259140, ext. 26394; Fax: +1 905 5229033; Email: guarnea{at}mcmaster.ca

Received January 9, 2009. Revised February 19, 2009. Accepted February 23, 2009.

SeqA is a negative regulator of DNA replication in Escherichia coli and related bacteria that functions by sequestering the origin of replication and facilitating its resetting after every initiation event. Inactivation of the seqA gene leads to unsynchronized rounds of replication, abnormal localization of nucleoids and increased negative superhelicity. Excess SeqA also disrupts replication synchrony and affects cell division. SeqA exerts its functions by binding clusters of transiently hemimethylated GATC sequences generated during replication. However, the molecular mechanisms that trigger formation and disassembly of such complex are unclear. We present here the crystal structure of a dimeric mutant of SeqA [SeqA{Delta}(41–59)-A25R] bound to tandem hemimethylated GATC sites. The structure delineates how SeqA forms a high-affinity complex with DNA and it suggests why SeqA only recognizes GATC sites at certain spacings. The SeqA–DNA complex also unveils additional protein–protein interaction surfaces that mediate the formation of higher ordered complexes upon binding to newly replicated DNA. Based on this data, we propose a model describing how SeqA interacts with newly replicated DNA within the origin of replication and at the replication forks.


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