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Hda inactivation of DnaA is the predominant mechanism preventing hyperinitiation of Escherichia coli DNA replication
Author(s) -
Camara Johanna E,
Breier Adam M,
Brendler Therese,
Austin Stuart,
Cozzarelli Nicholas R,
Crooke Elliott
Publication year - 2005
Publication title -
embo reports
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 4.584
H-Index - 184
eISSN - 1469-3178
pISSN - 1469-221X
DOI - 10.1038/sj.embor.7400467
Subject(s) - dnaa , seqa protein domain , biology , pre replication complex , dna replication , escherichia coli , origin of replication , microbiology and biotechnology , control of chromosome duplication , dna , replication factor c , dnab helicase , genetics , gene , rna , helicase
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.