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Deinococcus radiodurans — the consummate survivor

Nature Reviews Microbiology volume 3, pages 882–892 (2005)Cite this article

Key Points

  • Deinococcus radiodurans is distinguished by its extraordinary capacity to survive high levels of ionizing radiation, and the DNA double-strand breaks that result from exposure to this type of radiation.

  • There are radiation-resistant bacteria in several phyla, including members of the Archaea.

  • Radiation resistance seems to be mediated by passive and active (enzymatic) mechanisms.

  • Passive mechanisms include the presence of multiple genome copies, a highly condensed nucleoid organization that prevents diffusion of DNA fragments generated during irradiation, and an accumulation of Mn(II) ions that might prevent the generation of reactive oxygen species.

  • Enzymatic mechanisms of radiation resistance include conventional DNA-repair processes as well as novel functions.

  • Mechanisms for limiting the extent of DNA degradation post-irradiation seem to facilitate genome preservation and enhance radiation resistance.

  • There are several enzymatic pathways for the repair of double-strand breaks, including RecA-dependent and RecA-independent processes.

Abstract

Relatively little is known about the biochemical basis of the capacity of Deinococcus radiodurans to endure the genetic insult that results from exposure to ionizing radiation and can include hundreds of DNA double-strand breaks. However, recent reports indicate that this species compensates for extensive DNA damage through adaptations that allow cells to avoid the potentially detrimental effects of DNA strand breaks. It seems that D. radiodurans uses mechanisms that limit DNA degradation and that restrict the diffusion of DNA fragments that are produced following irradiation, to preserve genetic integrity. These mechanisms also increase the efficiency of the DNA-repair proteins.

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Figure 1: Potential contributions to the recovery from radiation damage in Deinococcus radiodurans.
Figure 2: A 16S-rRNA-gene-sequence-based phylogeny of the main lineages of the domain Bacteria.
Figure 3: A tetrad of Deinococcus radiodurans.
Figure 4: Synthesis-dependent strand annealing.
Figure 5: Inverse DNA-strand exchange promoted by the Deinococcus radiodurans RecA protein.
Figure 6: A proposed mechanism that might contribute to the tolerance of radiation damage in Deinococcus radiodurans.

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Acknowledgements

Work on genome repair in Deinococcus radiodurans in the Battista and Cox laboratories is supported a grant from the National Institutes of Health. The authors thank F.A. Rainey for producing the phylogenetic tree in Figure 2. We also thank J. Haber for helpful discussions.

Author information

Authors and Affiliations

  1. Department of Biochemistry, University of Wisconsin–Madison, Wisconsin, 53706-1544, USA

    Michael M. Cox

  2. Department of Biological Sciences, Louisiana State University and A&M College, Baton Rouge, 70803, Louisiana, USA

    John R. Battista

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  1. Michael M. Cox
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Correspondence to John R. Battista.

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DATABASES

Entrez

Azotobacter vinelandii

Bacillus subtilis

Deinococcus geothermalis

Deinococcus radiodurans strain R1

E. coli K12

Kineococcus radiotolerans

Lactobacillus plantarum

Rubrobacter xylanophilus

SwissProt

DNA polymerase I

D. radiodurans RecA

D. radiodurans SSB

E. coli RecA

E. coli SSB

PprA

RecR

FURTHER INFORMATION

John Battista's laboratory

Michael Cox's laboratory

Speculation on the origins of D. radiodurans

TIGR Comprehensive Microbial Resource database

Glossary

IONIZING RADIATION

Any electromagnetic or particulate radiation powerful enough to strip electrons from atoms to produce ions.

HYPERTHERMOPHILIC

Organisms that have an optimal growth temperature above 80°C.

EPISTASIS GROUP

This occurs when two or more genes control a phenotype. The combined effect of mutations in these genes on a phenotype deviates from the sum of their individual effects.

NON-HOMOLOGOUS END JOINING

One of several pathways that can be used to repair chromosomal double-strand DNA breaks. The process is non-homologous because adjacent broken strands are fused by direct end-to-end contact without regard to sequence homology. Therefore, non-homologous end joining is error-prone because it results in joining of the breaks without a template.

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Cox, M., Battista, J. Deinococcus radiodurans — the consummate survivor. Nat Rev Microbiol 3, 882–892 (2005). https://doi.org/10.1038/nrmicro1264

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