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Double-Strand DNA Break Repair in Mycobacteria

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  • Author: Michael S. Glickman1
  • Editors: Graham F. Hatfull2, William R. Jacobs Jr.3
  • VIEW AFFILIATIONS HIDE AFFILIATIONS
    Affiliations: 1: Immunology Program, Sloan Kettering Institute and Infectious Diseases, Memorial Sloan Kettering Cancer Center, 1275 York Ave., New York, NY 10065; 2: University of Pittsburgh, Pittsburgh, PA; 3: Howard Hughes Medical Institute, Albert Einstein College of Medicine, Bronx, NY
    • Source: microbiolspec September 2014 vol. 2 no. 5 doi:10.1128/microbiolspec.MGM2-0024-2013
  • Received 27 July 2013 Accepted 05 August 2013 Published 05 September 2014
  • M. S. Glickman, [email protected]
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  • Abstract:

    Discontinuity of both strands of the chromosome is a lethal event in all living organisms because it compromises chromosome replication. As such, a diversity of DNA repair systems has evolved to repair double-strand DNA breaks (DSBs). In part, this diversity of DSB repair systems has evolved to repair breaks that arise in diverse physiologic circumstances or sequence contexts, including cellular states of nonreplication or breaks that arise between repeats. Mycobacteria elaborate a set of three genetically distinct DNA repair pathways: homologous recombination, nonhomologous end joining, and single-strand annealing. As such, mycobacterial DSB repair diverges substantially from the standard model of prokaryotic DSB repair and represents an attractive new model system. In addition, the presence in mycobacteria of a DSB repair system that can repair DSBs in nonreplicating cells (nonhomologous end joining) or when DSBs arise between repeats (single-strand annealing) has clear potential relevance to pathogenesis, although the exact role of these systems in pathogenesis is still being elucidated. In this article we will review the genetics of mycobacterial DSB repair systems, focusing on recent insights.

  • Citation: Glickman M. 2014. Double-Strand DNA Break Repair in Mycobacteria. Microbiol Spectrum 2(5):MGM2-0024-2013. doi:10.1128/microbiolspec.MGM2-0024-2013.

References

1. Daley JM, Palmbos PL, Wu D, Wilson TE. 2005. Nonhomologous end joining in yeast. Annu Rev Genet 39:431–451. [PubMed][CrossRef]
2. Dillingham MS, Kowalczykowski SC. 2008. RecBCD enzyme and the repair of double-stranded DNA breaks. Microbiol Mol Biol Rev 72:642–671. [PubMed][CrossRef]
3. Lieber MR. 2010. The mechanism of double-strand DNA break repair by the nonhomologous DNA end-joining pathway. Annu Rev Biochem 79:181–211. [PubMed][CrossRef]
4. Shuman S, Glickman MS. 2007. Bacterial DNA repair by nonhomologous end joining. Nat Rev Microbiol 5:852–861. [PubMed][CrossRef]
5. Symington LS, Gautier J. 2011. Double-strand break end resection and repair pathway choice. Annu Rev Genet 45:247–271. [PubMed][CrossRef]
6. Yeeles JT, Dillingham MS. 2010. The processing of double-stranded DNA breaks for recombinational repair by helicase-nuclease complexes. DNA Repair 9:276–285. [PubMed][CrossRef]
7. Ford CB, Shah RR, Maeda MK, Gagneux S, Murray MB, Cohen T, Johnston JC, Gardy J, Lipsitch M, Fortune SM. 2013. Mycobacterium tuberculosis mutation rate estimates from different lineages predict substantial differences in the emergence of drug-resistant tuberculosis. Nat Genet 45:784–790. [PubMed][CrossRef]
8. Warner DF, Tonjum T, Mizrahi V. 2013. DNA metabolism in mycobacterial pathogenesis. Curr Top Microbiol Immunol 374:27–51. [PubMed][CrossRef]
9. Kurthkoti K, Varshney U. 2012. Distinct mechanisms of DNA repair in mycobacteria and their implications in attenuation of the pathogen growth. Mech Ageing Dev 133:138–146. [PubMed][CrossRef]
10. Gorna AE, Bowater RP, Dziadek J. 2010. DNA repair systems and the pathogenesis of Mycobacterium tuberculosis: varying activities at different stages of infection. Clin Sci 119:187–202. [PubMed][CrossRef]
11. Reijns MA, Rabe B, Rigby RE, Mill P, Astell KR, Lettice LA, Boyle S, Leitch A, Keighren M, Kilanowski F, Devenney PS, Sexton D, Grimes G, Holt IJ, Hill RE, Taylor MS, Lawson KA, Dorin JR, Jackson AP. 2012. Enzymatic removal of ribonucleotides from DNA is essential for mammalian genome integrity and development. Cell 149:1008–1022. [PubMed][CrossRef]
12. Hiller B, Achleitner M, Glage S, Naumann R, Behrendt R, Roers A. 2012. Mammalian RNase H2 removes ribonucleotides from DNA to maintain genome integrity. J Exp Med 209:1419–1426. [PubMed][CrossRef]
13. Wigley DB. 2013. Bacterial DNA repair: recent insights into the mechanism of RecBCD, AddAB and AdnAB. Nat Rev Microbiol 11:9–13. [PubMed][CrossRef]
14. Gupta R, Barkan D, Redelman-Sidi G, Shuman S, Glickman MS. 2011. Mycobacteria exploit three genetically distinct DNA double-strand break repair pathways. Mol Microbiol 79:316–330. [PubMed][CrossRef]
15. Stephanou NC, Gao F, Bongiorno P, Ehrt S, Schnappinger D, Shuman S, Glickman MS. 2007. Mycobacterial nonhomologous end joining mediates mutagenic repair of chromosomal double-strand DNA breaks. J Bacteriol 189:5237–5246. [PubMed][CrossRef]
16. Sinha KM, Unciuleac MC, Glickman MS, Shuman S. 2009. AdnAB: a new DSB-resecting motor-nuclease from mycobacteria. Genes Dev 23:1423–1437. [PubMed][CrossRef]
17. Fernandez S, Kobayashi Y, Ogasawara N, Alonso JC. 1999. Analysis of the Bacillus subtilis recO gene: RecO forms part of the RecFLOR function. Mol Gen Genet 261:567–573. [PubMed][CrossRef]
18. Gupta R, Ryzhikov M, Koroleva O, Unciuleac M, Shuman S, Korolev S, Glickman MS. 2013. A dual role for mycobacterial RecO in RecA-dependent homologous recombination and RecA-independent single-strand annealing. Nucleic Acids Res 41:2284–2295. [PubMed][CrossRef]
19. Patil KN, Singh P, Muniyappa K. 2011. DNA binding, coprotease, and strand exchange activities of mycobacterial RecA proteins: implications for functional diversity among RecA nucleoprotein filaments. Biochemistry 50:300–311. [PubMed][CrossRef]
20. Ganesh N, Muniyappa K. 2003. Characterization of DNA strand transfer promoted by Mycobacterium smegmatis RecA reveals functional diversity with Mycobacterium tuberculosis RecA. Biochemistry 42:7216–7225. [PubMed][CrossRef]
21. Datta S, Krishna R, Ganesh N, Chandra NR, Muniyappa K, Vijayan M. 2003. Crystal structures of Mycobacterium smegmatis RecA and its nucleotide complexes. J Bacteriol 185:4280–4284. [PubMed][CrossRef]
22. Reddy MS, Guhan N, Muniyappa K. 2001. Characterization of single-stranded DNA-binding proteins from mycobacteria. The carboxyl-terminal of domain of SSB is essential for stable association with its cognate RecA protein. J Biol Chem 276:45959–45968. [PubMed][CrossRef]
23. Dawson LF, Dillury J, Davis EO. 2010. RecA-independent DNA damage induction of Mycobacterium tuberculosis ruvC despite an appropriately located SOS box. J Bacteriol 192:599–603. [PubMed][CrossRef]
24. Yang M, Gao C, Cui T, An J, He ZG. 2012. A TetR-like regulator broadly affects the expressions of diverse genes in Mycobacterium smegmatis. Nucleic Acids Res 40:1009–1020. [PubMed][CrossRef]
25. Davis EO, Springer B, Gopaul KK, Papavinasasundaram KG, Sander P, Bottger EC. 2002. DNA damage induction of recA in Mycobacterium tuberculosis independently of RecA and LexA. Mol Microbiol 46:791–800. [PubMed][CrossRef]
26. Davis EO, Dullaghan EM, Rand L. 2002. Definition of the mycobacterial SOS box and use to identify LexA-regulated genes in Mycobacterium tuberculosis. J Bacteriol 184:3287–3295. [PubMed][CrossRef]
27. Brooks PC, Movahedzadeh F, Davis EO. 2001. Identification of some DNA damage-inducible genes of Mycobacterium tuberculosis: apparent lack of correlation with LexA binding. J Bacteriol 183:4459–4467. [PubMed][CrossRef]
28. Thakur RS, Basavaraju S, Somyajit K, Jain A, Subramanya S, Muniyappa K, Nagaraju G. 2013. Evidence for the role of Mycobacterium tuberculosis RecG helicase in DNA repair and recombination. FEBS J 280:1841–1860. [PubMed][CrossRef]
29. Prabu JR, Thamotharan S, Khanduja JS, Alipio EZ, Kim CY, Waldo GS, Terwilliger TC, Segelke B, Lekin T, Toppani D, Hung LW, Yu M, Bursey E, Muniyappa K, Chandra NR, Vijayan M. 2006. Structure of Mycobacterium tuberculosis RuvA, a protein involved in recombination. Acta Crystallogr Sect F Struct Biol Cryst Commun 62:731–734. [PubMed][CrossRef]
30. Khanduja JS, Muniyappa K. 2012. Functional analysis of DNA replication fork reversal catalyzed by Mycobacterium tuberculosis RuvAB proteins. J Biol Chem 287:1345–1360. [PubMed][CrossRef]
31. Khanduja JS, Tripathi P, Muniyappa K. 2009. Mycobacterium tuberculosis RuvA induces two distinct types of structural distortions between the homologous and heterologous Holliday junctions. Biochemistry 48:27–40. [PubMed][CrossRef]
32. Aravind L, Koonin EV. 2001. Prokaryotic homologs of the eukaryotic DNA-end-binding protein Ku, novel domains in the Ku protein and prediction of a prokaryotic double-strand break repair system. Genome Res 11:1365–1374. [PubMed][CrossRef]
33. Nandakumar J, Nair PA, Shuman S. 2007. Last stop on the road to repair: structure of E. coli DNA ligase bound to nicked DNA-adenylate. Mol Cell 26:257–271. [PubMed][CrossRef]
34. Della M, Palmbos PL, Tseng HM, Tonkin LM, Daley JM, Topper LM, Pitcher RS, Tomkinson AE, Wilson TE, Doherty AJ. 2004. Mycobacterial Ku and ligase proteins constitute a two-component NHEJ repair machine. Science 306:683–685. [PubMed][CrossRef]
35. Weller GR, Kysela B, Roy R, Tonkin LM, Scanlan E, Della M, Devine SK, Day JP, Wilkinson A, d’Adda di Fagagna F, Devine KM, Bowater RP, Jeggo PA, Jackson SP, Doherty AJ. 2002. Identification of a DNA nonhomologous end-joining complex in bacteria. Science 297:1686–1689. [PubMed][CrossRef]
36. Aniukwu J, Glickman MS, Shuman S. 2008. The pathways and outcomes of mycobacterial NHEJ depend on the structure of the broken DNA ends. Genes Dev 22:512–527. [PubMed][CrossRef]
37. Gong C, Bongiorno P, Martins A, Stephanou NC, Zhu H, Shuman S, Glickman MS. 2005. Mechanism of nonhomologous end-joining in mycobacteria: a low-fidelity repair system driven by Ku, ligase D and ligase C. Nat Struct Mol Biol 12:304–312. [PubMed][CrossRef]
38. Gong C, Martins A, Bongiorno P, Glickman M, Shuman S. 2004. Biochemical and genetic analysis of the four DNA ligases of mycobacteria. J Biol Chem 279:20594–20606. [PubMed][CrossRef]
39. Wang ST, Setlow B, Conlon EM, Lyon JL, Imamura D, Sato T, Setlow P, Losick R, Eichenberger P. 2006. The forespore line of gene expression in Bacillus subtilis. J Mol Biol 358:16–37. [PubMed][CrossRef]
40. Pitcher RS, Green AJ, Brzostek A, Korycka-Machala M, Dziadek J, Doherty AJ. 2007. NHEJ protects mycobacteria in stationary phase against the harmful effects of desiccation. DNA Repair 6:1271–1276. [PubMed][CrossRef]
41. Akey D, Martins A, Aniukwu J, Glickman MS, Shuman S, Berger JM. 2006. Crystal structure and nonhomologous end-joining function of the ligase component of mycobacterium DNA ligase D. J Biol Chem 281:13412–13423. [PubMed][CrossRef]
42. Pitcher RS, Brissett NC, Picher AJ, Andrade P, Juarez R, Thompson D, Fox GC, Blanco L, Doherty AJ. 2007. Structure and function of a mycobacterial NHEJ DNA repair polymerase. J Mol Biol 366:391–405. [PubMed][CrossRef]
43. Zhu H, Nandakumar J, Aniukwu J, Wang LK, Glickman MS, Lima CD, Shuman S. 2006. Atomic structure and nonhomologous end-joining function of the polymerase component of bacterial DNA ligase D. Proc Natl Acad Sci USA 103:1711–1716. [PubMed][CrossRef]
44. Bebenek K, Garcia-Diaz M, Patishall SR, Kunkel TA. 2005. Biochemical properties of Saccharomyces cerevisiae DNA polymerase IV. J Biol Chem 280:20051–20058. [PubMed][CrossRef]
45. Brissett NC, Pitcher RS, Juarez R, Picher AJ, Green AJ, Dafforn TR, Fox GC, Blanco L, Doherty AJ. 2007. Structure of a NHEJ polymerase-mediated DNA synaptic complex. Science 318:456–459. [PubMed][CrossRef]
46. Nair PA, Smith P, Shuman S. 2010. Structure of bacterial LigD 3′-phosphoesterase unveils a DNA repair superfamily. Proc Natl Acad Sci USA 107:12822–12827. [PubMed][CrossRef]
47. Zhu H, Shuman S. 2006. Substrate specificity and structure-function analysis of the 3′-phosphoesterase component of the bacterial NHEJ protein, DNA ligase D. J Biol Chem 281:13873–13881. [PubMed][CrossRef]
48. Zhu H, Wang LK, Shuman S. 2005. Essential constituents of the 3′-phosphoesterase domain of bacterial DNA ligase D, a nonhomologous end-joining enzyme. J Biol Chem 280:33707–33715. [PubMed][CrossRef]
49. Zhu H, Shuman S. 2005. Novel 3′-ribonuclease and 3′-phosphatase activities of the bacterial non-homologous end-joining protein, DNA ligase D. J Biol Chem 280:25973–25981. [PubMed][CrossRef]
50. Zhu H, Bhattarai H, Yan HG, Shuman S, Glickman MS. 2012. Characterization of Mycobacterium smegmatis PolD2 and PolD1 as RNA/DNA polymerases homologous to the POL domain of bacterial DNA ligase D. Biochemistry 51:10147–10158. [PubMed][CrossRef]
51. Sinha KM, Stephanou NC, Gao F, Glickman MS, Shuman S. 2007. Mycobacterial UvrD1 is a Ku-dependent DNA helicase that plays a role in multiple DNA repair events, including double-strand break repair. J Biol Chem 282:15114–15125. [PubMed][CrossRef]
52. Li Z, Wen J, Lin Y, Wang S, Xue P, Zhang Z, Zhou Y, Wang X, Sui L, Bi LJ, Zhang XE. 2011. A Sir2-like protein participates in mycobacterial NHEJ. PloS One 6:e20045. [PubMed][CrossRef]
53. Ivanov EL, Sugawara N, Fishman-Lobell J, Haber JE. 1996. Genetic requirements for the single-strand annealing pathway of double-strand break repair in Saccharomyces cerevisiae. Genetics 142:693–704. [PubMed]
54. McEvoy CR, Cloete R, Muller B, Schurch AC, van Helden PD, Gagneux S, Warren RM, Gey van Pittius NC. 2012. Comparative analysis of Mycobacterium tuberculosis pe and ppe genes reveals high sequence variation and an apparent absence of selective constraints. PloS One 7:e30593. [PubMed][CrossRef]
55. McEvoy CR, van Helden PD, Warren RM, Gey van Pittius NC. 2009. Evidence for a rapid rate of molecular evolution at the hypervariable and immunogenic Mycobacterium tuberculosis PPE38 gene region. BMC Evol Biol 9:237. [PubMed][CrossRef]
56. Talarico S, Cave MD, Marrs CF, Foxman B, Zhang L, Yang Z. 2005. Variation of the Mycobacterium tuberculosis PE_PGRS 33 gene among clinical isolates. J Clin Microbiol 43:4954–4960. [PubMed][CrossRef]
57. Talarico S, Zhang L, Marrs CF, Foxman B, Cave MD, Brennan MJ, Yang Z. 2008. Mycobacterium tuberculosis PE_PGRS16 and PE_PGRS26 genetic polymorphism among clinical isolates. Tuberculosis 88:283–294. [PubMed][CrossRef]
58. Wojcik EA, Brzostek A, Bacolla A, Mackiewicz P, Vasquez KM, Korycka-Machala M, Jaworski A, Dziadek J. 2012. Direct and inverted repeats elicit genetic instability by both exploiting and eluding DNA double-strand break repair systems in mycobacteria. PloS One 7:e51064. [PubMed][CrossRef]
59. Darwin KH, Ehrt S, Gutierrez-Ramos JC, Weich N, Nathan CF. 2003. The proteasome of Mycobacterium tuberculosis is required for resistance to nitric oxide. Science 302:1963–1966. [PubMed][CrossRef]
60. Darwin KH, Nathan CF. 2005. Role for nucleotide excision repair in virulence of Mycobacterium tuberculosis. Infect Immun 73:4581–4587. [PubMed][CrossRef]
61. Houghton J, Townsend C, Williams AR, Rodgers A, Rand L, Walker KB, Bottger EC, Springer B, Davis EO. 2012. Important role for Mycobacterium tuberculosis UvrD1 in pathogenesis and persistence apart from its function in nucleotide excision repair. J Bacteriol 194:2916–2923. [PubMed][CrossRef]
62. Sinha KM, Stephanou NC, Unciuleac MC, Glickman MS, Shuman S. 2008. Domain requirements for DNA unwinding by mycobacterial UvrD2, an essential DNA helicase. Biochemistry 47:9355–9364. [PubMed][CrossRef]
63. Williams A, Guthlein C, Beresford N, Bottger EC, Springer B, Davis EO. 2011. UvrD2 is essential in Mycobacterium tuberculosis, but its helicase activity is not required. J Bacteriol 193:4487–4494. [PubMed][CrossRef]
64. Boshoff HI, Reed MB, Barry CE, 3rd, Mizrahi V. 2003. DnaE2 polymerase contributes to in vivo survival and the emergence of drug resistance in Mycobacterium tuberculosis. Cell 113:183–193. [CrossRef]
65. Sander P, Papavinasasundaram KG, Dick T, Stavropoulos E, Ellrott K, Springer B, Colston MJ, Bottger EC. 2001. Mycobacterium bovis BCG recA deletion mutant shows increased susceptibility to DNA-damaging agents but wild-type survival in a mouse infection model. Infect Immun 69:3562–3568. [PubMed][CrossRef]
66. Harper J, Skerry C, Davis SL, Tasneen R, Weir M, Kramnik I, Bishai WR, Pomper MG, Nuermberger EL, Jain SK. 2012. Mouse model of necrotic tuberculosis granulomas develops hypoxic lesions. J Infect Dis 205:595–602. [PubMed][CrossRef]
67. Gill WP, Harik NS, Whiddon MR, Liao RP, Mittler JE, Sherman DR. 2009. A replication clock for Mycobacterium tuberculosis. Nat Med 15:211–214. [PubMed][CrossRef]
68. Kana BD, Abrahams GL, Sung N, Warner DF, Gordhan BG, Machowski EE, Tsenova L, Sacchettini JC, Stoker NG, Kaplan G, Mizrahi V. 2010. Role of the DinB homologs Rv1537 and Rv3056 in Mycobacterium tuberculosis. J Bacteriol 192:2220–2227. [PubMed][CrossRef]
69. Ford CB, Lin PL, Chase MR, Shah RR, Iartchouk O, Galagan J, Mohaideen N, Ioerger TR, Sacchettini JC, Lipsitch M, Flynn JL, Fortune SM. 2011. Use of whole genome sequencing to estimate the mutation rate of Mycobacterium tuberculosis during latent infection. Nat Genet 43:482–486. [PubMed][CrossRef]
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2014-09-05
2020-07-12

Abstract:

Discontinuity of both strands of the chromosome is a lethal event in all living organisms because it compromises chromosome replication. As such, a diversity of DNA repair systems has evolved to repair double-strand DNA breaks (DSBs). In part, this diversity of DSB repair systems has evolved to repair breaks that arise in diverse physiologic circumstances or sequence contexts, including cellular states of nonreplication or breaks that arise between repeats. Mycobacteria elaborate a set of three genetically distinct DNA repair pathways: homologous recombination, nonhomologous end joining, and single-strand annealing. As such, mycobacterial DSB repair diverges substantially from the standard model of prokaryotic DSB repair and represents an attractive new model system. In addition, the presence in mycobacteria of a DSB repair system that can repair DSBs in nonreplicating cells (nonhomologous end joining) or when DSBs arise between repeats (single-strand annealing) has clear potential relevance to pathogenesis, although the exact role of these systems in pathogenesis is still being elucidated. In this article we will review the genetics of mycobacterial DSB repair systems, focusing on recent insights.

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Double-Strand DNA Break Repair in Mycobacteria
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Citation: Glickman M. 2014. Double-strand dna break repair in mycobacteria. microbiolspec 2(5): doi:10.1128/microbiolspec.MGM2-0024-2013
/content/microbiolspec/10.1128/microbiolspec.MGM2-0024-2013.fig1
FIGURE 1
Pathways of DSB repair in mycobacteria. Our present understanding of DSB repair in mycobacteria. The three pathways shown are HR, NHEJ, and SSA. For each pathway, the major DNA processing events are depicted with the factors required for each step, when known. A question mark indicates that no specific experimental genetic data is available about that step, despite the presence of predicted proteins in mycobacterial chromosomes that may mediate these steps, or even biochemical activities consistent with a role in these pathways. In the NHEJ column the three outcomes below the arrow indicate faithful repair, nucleotide addition, and nucleotide trimming, respectively. In the SSA column, the blue rectangles indicate repeat sequences that flank the DSB. Please see text for further details and references.
microbiolspec/2/5/MGM2-0024-2013-fig1_thmb.gif
microbiolspec/2/5/MGM2-0024-2013-fig1.gif
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FIGURE 1

Pathways of DSB repair in mycobacteria. Our present understanding of DSB repair in mycobacteria. The three pathways shown are HR, NHEJ, and SSA. For each pathway, the major DNA processing events are depicted with the factors required for each step, when known. A question mark indicates that no specific experimental genetic data is available about that step, despite the presence of predicted proteins in mycobacterial chromosomes that may mediate these steps, or even biochemical activities consistent with a role in these pathways. In the NHEJ column the three outcomes below the arrow indicate faithful repair, nucleotide addition, and nucleotide trimming, respectively. In the SSA column, the blue rectangles indicate repeat sequences that flank the DSB. Please see text for further details and references.

Source: microbiolspec September 2014 vol. 2 no. 5 doi:10.1128/microbiolspec.MGM2-0024-2013
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Double-Strand DNA Break Repair in Mycobacteria
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Citation: Glickman M. 2014. Double-strand dna break repair in mycobacteria. microbiolspec 2(5): doi:10.1128/microbiolspec.MGM2-0024-2013
/content/microbiolspec/10.1128/microbiolspec.MGM2-0024-2013.T1
TABLE 1
Comparison of DSB repair systems in bacteria and yeast
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TABLE 1

Comparison of DSB repair systems in bacteria and yeast

Source: microbiolspec September 2014 vol. 2 no. 5 doi:10.1128/microbiolspec.MGM2-0024-2013

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