Hda inactivation of DnaA is the predominant mechanism preventing hyperinitiation of Escherichia coli DNA replication

Initiation of DNA replication from the Escherichia coli chromosomal origin is highly regulated, assuring that replication occurs precisely once per cell cycle. Three mechanisms for regulation of replication initiation have been proposed: titration of free DnaA initiator protein by the datA locus, se...

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Bibliographic Details
Published in:EMBO reports 2005-08, Vol.6 (8), p.736-741
Main Authors: Camara, Johanna E, Breier, Adam M, Brendler, Therese, Austin, Stuart, Cozzarelli, Nicholas R, Crooke, Elliott
Format: Article
Language:English
Subjects:
Adenosine diphosphate
Adenosine Triphosphatases - genetics
Adenosine Triphosphatases - physiology
Adenosine Triphosphate - chemistry
Alleles
ATP
Bacterial Physiological Phenomena
Bacterial Proteins - metabolism
Cell Cycle
Cell Proliferation
Deoxyribonucleic acid
DNA
DNA - chemistry
DNA Replication
DNA-Binding Proteins - chemistry
DNA-Binding Proteins - metabolism
DnaA
E coli
Escherichia coli
Escherichia coli - genetics
Escherichia coli - metabolism
Escherichia coli Proteins - genetics
Escherichia coli Proteins - physiology
Flow Cytometry
Gene Expression Regulation, Bacterial
Genes, Bacterial
Genotype
Hda
Immunoblotting
Inactivation
initiation
Light
Models, Genetic
Multiprotein Complexes
Mutation
Oligonucleotide Array Sequence Analysis
oriC
replication
Replication Origin
Scattering, Radiation
Scientific Report
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Summary:Initiation of DNA replication from the Escherichia coli chromosomal origin is highly regulated, assuring that replication occurs precisely once per cell cycle. Three mechanisms for regulation of replication initiation have been proposed: titration of free DnaA initiator protein by the datA locus, sequestration of newly replicated origins by SeqA protein and regulatory inactivation of DnaA (RIDA), in which active ATP‐DnaA is converted to the inactive ADP‐bound form. DNA microarray analyses showed that the level of initiation in rapidly growing cells that lack datA was indistinguishable from that in wild‐type cells, and that the absence of SeqA protein caused only a modest increase in initiation, in agreement with flow‐cytometry data. In contrast, cells lacking Hda overinitiated replication twofold, implicating RIDA as the predominant mechanism preventing extra initiation events in a cell cycle.
ISSN:1469-221X
1469-3178
1469-221X
DOI:10.1038/sj.embor.7400467