Postreplication repair

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Postreplication repair is the repair of damage to the DNA that takes place after replication.

Some example genes in humans include:

DNA damage prevents the normal enzymatic synthesis of DNA by the replication fork.[1][2][3][4] At damaged sites in the genome, both prokaryotic and eukaryotic cells utilize a number of postreplication repair (PRR) mechanisms to complete DNA replication. Chemically modified bases can be bypassed by either error-prone[5] or error-free[6] translesion polymerases, or through genetic exchange with the sister chromatid.[7] The replication of DNA with a broken sugar-phosphate backbone is most likely facilitated by the homologous recombination proteins that confer resistance to ionizing radiation. The activity of PRR enzymes is regulated by the SOS response in bacteria and may be controlled by the postreplication checkpoint response in eukaryotes.[8][9]

The elucidation of PRR mechanisms is an active area of molecular biology research, and the terminology is currently in flux. For instance, PRR has recently been referred to as "DNA damage tolerance" to emphasize the instances in which postreplication DNA damage is repaired without removing the original chemical modification to the DNA.[10] While the term PRR has most frequently been used to describe the repair of single-stranded postreplication gaps opposite damaged bases, a more broad usage has been suggested.[8] In this case, the term PRR would encompasses all processes that facilitate the replication of damaged DNA, including those that repair replication-induced double-strand breaks.

References[edit]

  1. ^ Rupp WD, Howard-Flanders P. Discontinuities in the DNA synthesized in an excision-defective strain of Escherichia coli following ultraviolet irradiation. J Mol Biol 1968; 31:291-304.
  2. ^ Lehmann AR. Post-replication repair of DNA in ultraviolet-irradiated mammalian cells. No gaps in DNA synthesized late after ultraviolet irradiation. Eur J Biochem 1972; 31:438-45.
  3. ^ di Caprio L, Cox BS. DNA synthesis in UV-irradiated yeast. Mutat Res 1981; 82:69-85.
  4. ^ Prakash L. Characterization of postreplication repair in Saccharomyces cerevisiae and effects of rad6, rad18, rev3 and rad52 mutations. Mol Gen Genet 1981; 184:471-8
  5. ^ Morrison A, Christensen RB, Alley J, Beck AK, Bernstine EG, Lemontt JF, Lawrence CW.REV3, a Saccharomyces cerevisiae gene whose function is required for induced mutagenesis, is predicted to encode a nonessential DNA polymerase. Journal Of Bacteriology 1989; 171:5659-67/
  6. ^ Masutani C, Kusumoto R, Yamada A, Dohmae N, Yokoi M, Yuasa M, Araki M, Iwai S, Takio K, Hanaoka F. The XPV (xeroderma pigmentosum variant) gene encodes human DNA polymerase eta. Nature 1999; 399:700-4.
  7. ^ Zhang H, Lawrence CW. The error-free component of the RAD6/RAD18 DNA damage tolerance pathway of budding yeast employs sister-strand recombination. Proc Natl Acad Sci U S A 2005; 102:15954-9.
  8. ^ a b Callegari AJ, Kelly TJ. Shedding light on the DNA damage checkpoint. Cell Cycle 2007; 6:660-6.
  9. ^ Lopes M, Foiani M, Sogo JM. Multiple mechanisms control chromosome integrity after replication fork uncoupling and restart at irreparable UV lesions. Mol Cell 2006; 21:15-27.
  10. ^ Friedberg EC. "Suffering in silence: the tolerance of DNA damage." Nat Rev Mol Cell Biol 2005; 6:943-53.