Bacterial Proliferation: Keep Dividing and Don't Mind the Gap

• Published in: PLoS genetics Vol. 11; no. 12; p. e1005757
• Main Authors: Laureti, Luisa, Demol, Julien, Fuchs, Robert P, Pagès, Vincent
• Format: Journal Article
• Language: English
• Published: United States Public Library of Science 01-12-2015; Public Library of Science (PLoS)
• Subjects: Biochemistry, Molecular Biology; Cell Division; Cell proliferation; Chromosomes; DNA Breaks, Single-Stranded; DNA Damage; DNA repair; DNA sequencing; Escherichia coli - genetics; Escherichia coli - physiology; Escherichia coli Proteins - genetics; Escherichia coli Proteins - metabolism; Life Sciences; Methods; Molecular biology; Nucleotide sequencing; Observations; Plasmids; Rec A Recombinases - genetics; Rec A Recombinases - metabolism; Recombinational DNA Repair
• ISSN: 1553-7404; 1553-7390; 1553-7404
• DOI: 10.1371/journal.pgen.1005757

DNA Damage Tolerance (DDT) mechanisms help dealing with unrepaired DNA lesions that block replication and challenge genome integrity. Previous in vitro studies showed that the bacterial replicase is able to re-prime downstream of a DNA lesion, leaving behind a single-stranded DNA gap. The question remains of what happens to this gap in vivo. Following the insertion of a single lesion in the chromosome of a living cell, we showed that this gap is mostly filled in by Homology Directed Gap Repair in a RecA dependent manner. When cells fail to repair this gap, or when homologous recombination is impaired, cells are still able to divide, leading to the loss of the damaged chromatid, suggesting that bacteria lack a stringent cell division checkpoint mechanism. Hence, at the expense of losing one chromatid, cell survival and proliferation are ensured.