Justin Courcelle

Answering the Call: Coping with DNA Damage at the Most Inopportune Time.

DNA damage-induced replication fork regression and processing in Escherichia coli.

RecA-dependent recovery of arrested DNA replication forks.

RecO acts with RecF and RecR to protect and maintain replication forks blocked by UV-induced DNA damage in Escherichia coli.

RuvAB and RecG are not essential for the recovery of DNA synthesis following UV-induced DNA damage in Escherichia coli.

When replication travels on damaged templates: bumps and blocks in the road.

Recs preventing wrecks.

Nucleotide excision repair or polymerase V-mediated lesion bypass can act to restore UV-arrested replication forks in Escherichia coli.

Nascent DNA processing by RecJ favors lesion repair over translesion synthesis at arrested replication forks in Escherichia coli.

Monitoring DNA replication following UV-induced damage in Escherichia coli.

RuvABC is required to resolve holliday junctions that accumulate following replication on damaged templates in Escherichia coli.

Structural conservation of RecF and Rad50: implications for DNA recognition and RecF function.

Inactivation of the DnaB helicase leads to the collapse and degradation of the replication fork: a comparison to UV-induced arrest.

RecBCD and RecJ/RecQ initiate DNA degradation on distinct substrates in UV-irradiated Escherichia coli.

RecA433 cells are defective in recF-mediated processing of disrupted replication forks but retain recBCD-mediated functions.

Shifting replication between IInd, IIIrd, and IVth gears.

Nucleotide excision repair is a predominant mechanism for processing nitrofurazone-induced DNA damage in Escherichia coli.

ATP binding, ATP hydrolysis, and protein dimerization are required for RecF to catalyze an early step in the processing and recovery of replication forks disrupted by DNA damage.

Escherichia coli Fpg glycosylase is nonrendundant and required for the rapid global repair of oxidized purine and pyrimidine damage in vivo.