Titration of the Escherichia coli DnaA protein to excess datA sites causes destabilization of replication forks, delayed replication initiation and delayed cell division
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Titration of the Escherichia coli DnaA protein to excess datA sites causes destabilization of replication forks, delayed replication initiation and delayed cell division. / Morigen, ; Løbner-Olesen, Anders; Skarstad, Kirsten.
I: Molecular Microbiology, Bind 50, Nr. 1, 2003, s. 349-362.Publikation: Bidrag til tidsskrift › Tidsskriftartikel › Forskning › fagfællebedømt
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TY - JOUR
T1 - Titration of the Escherichia coli DnaA protein to excess datA sites causes destabilization of replication forks, delayed replication initiation and delayed cell division
AU - Morigen, null
AU - Løbner-Olesen, Anders
AU - Skarstad, Kirsten
PY - 2003
Y1 - 2003
N2 - In Escherichia coli, the level of the initiator protein DnaA is limiting for initiation of replication at oriC. A high-affinity binding site for DnaA, datA, plays an important role. Here, the effect of extra datA sites was studied. A moderate increase in datA dosage ( approximately fourfold) delayed initiation of replication and cell division, but increased the rate of replication fork movement about twofold. At a further increase in the datA gene dosage, the SOS response was induced, and incomplete rounds of chromosome replication were detected. Overexpression of DnaA protein suppressed the SOS response and restored normal replication timing and rate of fork movement. In the presence of extra datA sites, cells showed a dependency on PriA and RecA proteins, indicating instability of the replication fork. The results suggest that wild-type replication fork progression normally includes controlled pausing, and that this is a prerequisite for normal replication fork function.
AB - In Escherichia coli, the level of the initiator protein DnaA is limiting for initiation of replication at oriC. A high-affinity binding site for DnaA, datA, plays an important role. Here, the effect of extra datA sites was studied. A moderate increase in datA dosage ( approximately fourfold) delayed initiation of replication and cell division, but increased the rate of replication fork movement about twofold. At a further increase in the datA gene dosage, the SOS response was induced, and incomplete rounds of chromosome replication were detected. Overexpression of DnaA protein suppressed the SOS response and restored normal replication timing and rate of fork movement. In the presence of extra datA sites, cells showed a dependency on PriA and RecA proteins, indicating instability of the replication fork. The results suggest that wild-type replication fork progression normally includes controlled pausing, and that this is a prerequisite for normal replication fork function.
KW - Adenosine Triphosphatases/genetics
KW - Bacterial Outer Membrane Proteins
KW - Bacterial Proteins/metabolism
KW - Cell Division
KW - DNA Helicases/genetics
KW - DNA Replication
KW - DNA, Bacterial/metabolism
KW - DNA-Binding Proteins/metabolism
KW - Escherichia coli/cytology
KW - Escherichia coli Proteins/genetics
KW - Exodeoxyribonuclease V/genetics
KW - Gene Dosage
KW - Gene Expression Regulation, Bacterial
KW - Protein Binding
KW - Rec A Recombinases/genetics
KW - Replication Origin
KW - SOS Response (Genetics)
KW - Suppression, Genetic
KW - Transcription Factors/genetics
KW - Transformation, Bacterial
KW - Ultraviolet Rays
U2 - 10.1046/j.1365-2958.2003.03695.x
DO - 10.1046/j.1365-2958.2003.03695.x
M3 - Journal article
C2 - 14507385
VL - 50
SP - 349
EP - 362
JO - Molecular Microbiology
JF - Molecular Microbiology
SN - 0950-382X
IS - 1
ER -
ID: 200972144