This Article Full Text Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Services Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Copyright Information Books from ASM Press MicrobeWorld Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Courcelle, J. Articles by Hanawalt, P. C. Search for Related Content PubMed PubMed Citation Articles by Courcelle, J. Articles by Hanawalt, P. C.

Journal of Bacteriology, February 1999, p. 916-922, Vol. 181, No. 3
0021-9193/99/$04.00+0
Copyright © 1999, American Society for Microbiology. All rights reserved.

Recovery of DNA Replication in UV-Irradiated Escherichia coli Requires both Excision Repair and RecF Protein Function

Justin Courcelle,^* David J. Crowley, and Philip C. Hanawalt

Department of Biological Sciences, Stanford University, Stanford, California 94305

Received 11 September 1998/Accepted 11 November 1998

After UV doses that disrupt DNA replication, the recovery of replication at replication forks in Escherichia coli requires a functional copy of the recF gene. In recF mutants, replication fails to recover and extensive degradation of the nascent DNA occurs, suggesting that recF function is needed to stabilize the disrupted replication forks and facilitate the process of recovery. We show here that the ability of recF to promote the recovery of replication requires that the disrupting lesions be removed. In the absence of excision repair, recF⁺ cells protect the nascent DNA at replication forks, but replication does not resume. The classical view is that recombination proteins operate in pathways that are independent from DNA repair, and therefore the functions of Rec proteins have been studied in repair-deficient cells. However, mutations in either uvr or recF result in failure to recover replication at UV doses from which wild-type cells recover efficiently, suggesting that recF and excision repair contribute to a common pathway in the recovery of replication.

---

^* Corresponding author. Mailing address: Department of Biological Sciences, Stanford University, Stanford, CA 94305-5020. Phone: (650) 723-2425. Fax: (650) 725-1848. E-mail: jcc{at}leland.stanford.edu.

This paper is dedicated to the memory of Tokio Kogoma. His work, comments, and insights have significantly contributed to the present work and will be missed in the future.

---

Journal of Bacteriology, February 1999, p. 916-922, Vol. 181, No. 3
0021-9193/99/$04.00+0
Copyright © 1999, American Society for Microbiology. All rights reserved.

This article has been cited by other articles:

• McInerney, P., O'Donnell, M. (2007). Replisome Fate upon Encountering a Leading Strand Block and Clearance from DNA by Recombination Proteins. J. Biol. Chem. 282: 25903-25916 [Abstract] [Full Text]  
• Belle, J. J., Casey, A., Courcelle, C. T., Courcelle, J. (2007). Inactivation of the DnaB Helicase Leads to the Collapse and Degradation of the Replication Fork: a Comparison to UV-Induced Arrest. J. Bacteriol. 189: 5452-5462 [Abstract] [Full Text]  
• Ni, M., Wang, S.-Y., Li, J.-K., Ouyang, Q. (2007). Simulating the Temporal Modulation of Inducible DNA Damage Response in Escherichia coli. Biophys. J 93: 62-73 [Abstract] [Full Text]  
• Shereda, R. D., Bernstein, D. A., Keck, J. L. (2007). A Central Role for SSB in Escherichia coli RecQ DNA Helicase Function. J. Biol. Chem. 282: 19247-19258 [Abstract] [Full Text]  
• Rudolph, C. J., Upton, A. L., Lloyd, R. G. (2007). Replication fork stalling and cell cycle arrest in UV-irradiated Escherichia coli. Genes Dev. 21: 668-681 [Abstract] [Full Text]  
• Ivancic-Bace, I., Vlasic, I., Cogelja-Cajo, G., Brcic-Kostic, K., Salaj-Smic, E. (2006). Roles of PriA Protein and Double-Strand DNA Break Repair Functions in UV-Induced Restriction Alleviation in Escherichia coli. Genetics 174: 2137-2149 [Abstract] [Full Text]  
• Donaldson, J. R., Courcelle, C. T., Courcelle, J. (2006). RuvABC Is Required to Resolve Holliday Junctions That Accumulate following Replication on Damaged Templates in Escherichia coli. J. Biol. Chem. 281: 28811-28821 [Abstract] [Full Text]  
• Goranov, A. I., Kuester-Schoeck, E., Wang, J. D., Grossman, A. D. (2006). Characterization of the Global Transcriptional Responses to Different Types of DNA Damage and Disruption of Replication in Bacillus subtilis.. J. Bacteriol. 188: 5595-5605 [Abstract] [Full Text]  
• Honda, M., Inoue, J., Yoshimasu, M., Ito, Y., Shibata, T., Mikawa, T. (2006). Identification of the RecR Toprim Domain as the Binding Site for both RecF and RecO: A ROLE OF RecR IN RecFOR ASSEMBLY AT DOUBLE-STRANDED DNA-SINGLE-STRANDED DNA JUNCTIONS. J. Biol. Chem. 281: 18549-18559 [Abstract] [Full Text]  
• Courcelle, C. T., Chow, K.-H., Casey, A., Courcelle, J. (2006). Nascent DNA processing by RecJ favors lesion repair over translesion synthesis at arrested replication forks in Escherichia coli. Proc. Natl. Acad. Sci. USA 103: 9154-9159 [Abstract] [Full Text]  
• Courcelle, C. T., Belle, J. J., Courcelle, J. (2005). Nucleotide Excision Repair or Polymerase V-Mediated Lesion Bypass Can Act To Restore UV-Arrested Replication Forks in Escherichia coli. J. Bacteriol. 187: 6953-6961 [Abstract] [Full Text]  
• Hishida, T., Han, Y.-W., Shibata, T., Kubota, Y., Ishino, Y., Iwasaki, H., Shinagawa, H. (2004). Role of the Escherichia coli RecQ DNA helicase in SOS signaling and genome stabilization at stalled replication forks. Genes Dev. 18: 1886-1897 [Abstract] [Full Text]  
• McInerney, P., O'Donnell, M. (2004). Functional Uncoupling of Twin Polymerases: MECHANISM OF POLYMERASE DISSOCIATION FROM A LAGGING-STRAND BLOCK. J. Biol. Chem. 279: 21543-21551 [Abstract] [Full Text]  
• Donaldson, J. R., Courcelle, C. T., Courcelle, J. (2004). RuvAB and RecG Are Not Essential for the Recovery of DNA Synthesis Following UV-Induced DNA Damage in Escherichia coli. Genetics 166: 1631-1640 [Abstract] [Full Text]  
• Chow, K.-H., Courcelle, J. (2004). RecO Acts with RecF and RecR to Protect and Maintain Replication Forks Blocked by UV-induced DNA Damage in Escherichia coli. J. Biol. Chem. 279: 3492-3496 [Abstract] [Full Text]  
• Bernstein, D. A., Keck, J. L. (2003). Domain mapping of Escherichia coli RecQ defines the roles of conserved N- and C-terminal regions in the RecQ family. Nucleic Acids Res 31: 2778-2785 [Abstract] [Full Text]  
• Courcelle, J., Donaldson, J. R., Chow, K.-H., Courcelle, C. T. (2003). DNA Damage-Induced Replication Fork Regression and Processing in Escherichia coli. Science 299: 1064-1067 [Abstract] [Full Text]  
• Grigorian, A. V., Lustig, R. B., Guzman, E. C., Mahaffy, J. M., Zyskind, J. W. (2003). Escherichia coli Cells with Increased Levels of DnaA and Deficient in Recombinational Repair Have Decreased Viability. J. Bacteriol. 185: 630-644 [Abstract] [Full Text]  
• Spek, E. J., Vuong, L. N., Matsuguchi, T., Marinus, M. G., Engelward, B. P. (2002). Nitric Oxide-Induced Homologous Recombination in Escherichia coli Is Promoted by DNA Glycosylases. J. Bacteriol. 184: 3501-3507 [Abstract] [Full Text]  
• Hanna, M. N., Ferguson, R. J., Li, Y.-H., Cvitkovitch, D. G. (2001). uvrA Is an Acid-Inducible Gene Involved in the Adaptive Response to Low pH in Streptococcus mutans. J. Bacteriol. 183: 5964-5973 [Abstract] [Full Text]  
• Courcelle, J., Hanawalt, P. C. (2001). Participation of recombination proteins in rescue of arrested replication forks in UV-irradiated Escherichia coli need not involve recombination. Proc. Natl. Acad. Sci. USA 98: 8196-8202 [Abstract] [Full Text]  
• Courcelle, J., Khodursky, A., Peter, B., Brown, P. O., Hanawalt, P. C. (2001). Comparative Gene Expression Profiles Following UV Exposure in Wild-Type and SOS-Deficient Escherichia coli. Genetics 158: 41-64 [Abstract] [Full Text]  
• Rangarajan, S., Woodgate, R., Goodman, M. F. (1999). A phenotype for enigmatic DNA polymerase II: A pivotal role for pol II in replication restart in UV-irradiated Escherichia coli. Proc. Natl. Acad. Sci. USA 96: 9224-9229 [Abstract] [Full Text]