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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, glickmam@mskcc.org
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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.

Key Concept Ranking

Bacterial Proteins
0.68154097
Nucleotide Excision Repair
0.5361176
Repetitive DNA
0.415071
0.68154097

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2014-09-05
2017-09-21

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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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. doi:10.1128/microbiolspec.MGM2-0024-2013.f1

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