Radiation Tolerance


Life on earth was not exposed to high‐dose ultraviolet (UV) light or ionising radiation (IR) until the last century. Despite this fact, it is possible to isolate species from within the Bacteria and Archaea that display an unusually high resistance to the lethal effects of UV light and/or IR when compared to the rest of the tree of life. Questions concerning what mechanisms mediate this radiation tolerance and why radiotolerance evolved in an environment void of sources of high‐energy radiation define the study of these species. A great deal is known concerning the specific biochemical and physiological processes that counteract the damage caused by electromagnetic radiations, but almost all species express the proteins that mediate these processes. The nature of what distinguishes a radioresistant species from a radiosensitive species remains elusive.

Key Concepts

  • A small subset of Bacteria and Archaea express unusually high resistance to the lethal effects of UV and ionising radiations.
  • Beyond experimental evaluation, there are no overt characteristics that predict radiation tolerance; species can be defined as radiation‐tolerant only empirically.
  • UV and ionising radiations kill by altering the DNA structure in a manner that interferes with the irradiated cell's ability to propagate.
  • A number of active and passive mechanisms are known to contribute to a species' radiation tolerance, but a comprehensive explanation for radioresistance in any single species has remained elusive.
  • Endospores tolerate UV and ionising radiations by mechanisms not available to their vegetative forms.
  • The flux of UV and ionising radiations on earth have never been great enough to explain why high‐level resistance to these stresses evolved; a number of hypotheses have been put forward to account for the existence of radioresistant phenotypes.

Keywords: radiation tolerance; radioresistance; UV light; ionising radiation; passive protection from DNA damage; enzymatic protection from DNA damage; endospore survival; panspermia; exaptation

Figure 1. Overview of excision repair processes. Native DNA can be damaged by a variety of physical and chemical agents. During an excision repair process, that damage is detected and the damaged base is removed from the DNA strand carrying the lesion. During base excision repair (BER), only the damaged base is removed, eventually resulting in a one base gap in the strand. During nucleotide excision repair (NER), a 12–13 base section of the strand containing the damage is removed. During alternative excision repair (AER), the strand is incised 5′ to the damaged base and the damage removed through nick translation from the site of the incision. Gaps formed are filled by a DNA polymerase and sealed by a DNA ligase, restoring the native DNA sequence.
Figure 2. Generation of a daughter strand gap. When a replicative polymerase reaches a bulky lesion (illustrated here as a thymine dimer) in the template strand, the polymerase dissociates from that strand and reinitiates DNA synthesis downstream of the lesion creating a daughter strand gap. The undamaged strand replicates normally. Parental DNA strands are represented as solid lines; daughter strands are dashed lines.
Figure 3. Daughter strand gap repair. A daughter strand gap can be resolved through RecA‐dependent homologous recombination between the sister DNA duplexes formed during replication. Isologous strands from the sisters exchange, creating a Holliday junction. This crossover is followed by branch migration and eventual resolution through incision at points a or b. Following resolution, there are two intact sister duplexes. The damage that caused the gap to form can then be repaired by excision repair. Parental DNA strands are represented as solid lines; daughter strands are dashed lines.
Figure 4. Translesion bypass. During trans‐lesion bypass, a blocked polymerase or daughter strand gap is sidestepped by a specialised DNA polymerase that can replicate through the blocking lesion. The process is error‐prone, as the base inserted opposite the lesion is not necessarily that which would pair with the damaged nucleotide in native DNA. Parental DNA strands are represented as solid lines; daughter strands are dashed lines.


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Battista, John R(May 2016) Radiation Tolerance. In: eLS. John Wiley & Sons Ltd, Chichester. http://www.els.net [doi: 10.1002/9780470015902.a0020365]