Abortive recombination in Escherichia coli ruv mutants blocks chromosome partitioning

Abstract

Background: All the ruvA, ruvB and ruvC mutants of Escherichia coli are sensitive to treatments that damage DNA, and are mildly defective in homologous recombination. It has been reported that the ruv mutants form nonseptate, multinuclear filaments after low doses of UV irradiation, dependent on the sfiA gene product. In vitro, the RuvAB complex promotes the branch migration of Holliday junctions, and RuvC resolves the junctions endonucleolytically.

The Evolution of Meiosis From Mitosis

“…We are also grateful to Richard D'Ari and Arthur Lesk for alerting us, respectively, to the results of Ishioka et al (1998) and the analysis of Lynch (2005).…”

“…The larger the genome size and the greater the number of chromosomes, the greater the chances of such events. It has been shown in E. coli that unresolved recombination events can indeed block chromosome segregation, leading to the production of filamentous cells (Ishioka et al 1998). In contemporary eukaryotic cells, such events are avoided through the use of DNA damage checkpoints, which halt chromosome separations until repair is achieved.…”

Promoting and Avoiding Recombination: Contrasting Activities of the Escherichia coli RuvABC Holliday Junction Resolvase and RecG DNA Translocase

“…Previous studies demonstrated that polA, dam, and uvrD strains lacking RuvABC are inviable and assumed the cells accumulate Holliday junctions that interfere with growth and division (Ishioka et al 1998;Marinus 2000;Flores et al 2005;Magner et al 2007). If true, it would imply that RecG does not provide an efficient alternative resolution pathway.…”

“…The evidence stems from studies in which we had initially exploited a synthetic lethality assay to screen for mutations incompatible with a deletion of ruvC. The seven mutations identified inactivated dam, polA, or uvrD (supporting information, File S1 and Figure S1), which previous studies had reported to be inviable with ruv (Ishioka et al 1998;Marinus 2000;Flores et al 2005;Magner et al 2007). The polA gene encodes Pol I, a DNA polymerase and exonuclease associated with nucleotide excision repair and the processing of Okazaki fragments during DNA replication , whereas the dam gene encodes a deoxyadenosine methylase that directs the MutHLS mismatch repair system to the newly synthesized strands (Modrich 1991).…”

“…With no means to distinguish parental strands from nascent strands, the MutHLS proteins initiate mismatch repair indiscriminately in dam mutants, which may result in chromosome breakage when repair tracks overlap ( Figure 1B). Thus, the viability of both polA and dam mutants depends on recombination proteins to repair DNA breaksRecBCD and RecA to initiate exchanges at the broken DNA ends and RuvABC to cleave Holliday junctions (Figure 1, A and B) (Lloyd et al 1974;Hong et al 1995;Kuzminov 1995;Ishioka et al 1998;Marinus 2000).…”