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 Previous Article

Molecular and Cellular Biology, November 2007, p. 7758-7764, Vol. 27, No. 21
0270-7306/07/$08.00+0     doi:10.1128/MCB.01331-07
Copyright © 2007, American Society for Microbiology. All Rights Reserved.

Requirement of RAD52 Group Genes for Postreplication Repair of UV-Damaged DNA in Saccharomyces cerevisiae{triangledown}

Venkateswarlu Gangavarapu, Satya Prakash, and Louise Prakash*

Department of Biochemistry and Molecular Biology, University of Texas Medical Branch, 301 University Blvd., Galveston, Texas 77555-1061

Received 24 July 2007/ Returned for modification 12 August 2007/ Accepted 23 August 2007

In Saccharomyces cerevisiae, replication through DNA lesions is promoted by Rad6-Rad18-dependent processes that include translesion synthesis by DNA polymerases {eta} and {zeta} and a Rad5-Mms2-Ubc13-controlled postreplicational repair (PRR) pathway which repairs the discontinuities in the newly synthesized DNA that form opposite from DNA lesions on the template strand. Here, we examine the contributions of the RAD51, RAD52, and RAD54 genes and of the RAD50 and XRS2 genes to the PRR of UV-damaged DNA. We find that deletions of the RAD51, RAD52, and RAD54 genes impair the efficiency of PRR and that almost all of the PRR is inhibited in the absence of both Rad5 and Rad52. We suggest a role for the Rad5 pathway when the lesion is located on the leading strand template and for the Rad52 pathway when the lesion is located on the lagging strand template. We surmise that both of these pathways operate in a nonrecombinational manner, Rad5 by mediating replication fork regression and template switching via its DNA helicase activity and Rad52 via a synthesis-dependent strand annealing mode. In addition, our results suggest a role for the Rad50 and Xrs2 proteins and thereby for the MRX complex in promoting PRR via both the Rad5 and Rad52 pathways.

* Corresponding author. Mailing address: University of Texas Medical Branch at Galveston, 301 University Blvd., Galveston, TX 77555-1061. Phone: (409) 747-8601. Fax: (409) 747-8608. E-mail: l.prakash{at}utmb.edu

{triangledown} Published ahead of print on 4 September 2007.

Molecular and Cellular Biology, November 2007, p. 7758-7764, Vol. 27, No. 21
0270-7306/07/$08.00+0     doi:10.1128/MCB.01331-07
Copyright © 2007, American Society for Microbiology. All Rights Reserved.



This article has been cited by other articles:

  • Adar, S., Izhar, L., Hendel, A., Geacintov, N., Livneh, Z. (2009). Repair of gaps opposite lesions by homologous recombination in mammalian cells. Nucleic Acids Res 37: 5737-5748 [Abstract] [Full Text]  
  • Pages, V., Santa Maria, S. R., Prakash, L., Prakash, S. (2009). Role of DNA damage-induced replication checkpoint in promoting lesion bypass by translesion synthesis in yeast. Genes Dev. 23: 1438-1449 [Abstract] [Full Text]  
  • Mito, E., Mokhnatkin, J. V., Steele, M. C., Buettner, V. L., Sommer, S. S., Manthey, G. M., Bailis, A. M. (2008). Mutagenic and Recombinagenic Responses to Defective DNA Polymerase {delta} Are Facilitated by the Rev1 Protein in pol3-t Mutants of Saccharomyces cerevisiae. Genetics 179: 1795-1806 [Abstract] [Full Text]  
  • Santa Maria, S. R., Gangavarapu, V., Johnson, R. E., Prakash, L., Prakash, S. (2007). Requirement of Nse1, a Subunit of the Smc5-Smc6 Complex, for Rad52-Dependent Postreplication Repair of UV-Damaged DNA in Saccharomyces cerevisiae. Mol. Cell. Biol. 27: 8409-8418 [Abstract] [Full Text]  


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