Non-bulky Lesions in Human DNA: the Ways of Formation, Repair, and Replication

A V Ignatov1,2, K A Bondarenko1, A V Makarova1

  • 1Institute of Molecular Genetics of Russian Academy of Sciences, Kurchatov sq. 2, Moscow, 123182 , Russia.

Acta Naturae
|November 7, 2017
PubMed

Insights

DNA damage can halt DNA replication, but specialized DNA polymerases help cells tolerate it. These enzymes efficiently synthesize DNA across lesions, though with lower accuracy, aiding survival.

Area of Science:

  • Molecular Biology
  • Genetics
  • Biochemistry

Background:

  • DNA damage is a significant threat to genomic integrity, potentially causing replication interruption, mutations, and cell death.
  • Cells possess multiple DNA repair pathways to counteract DNA damage.
  • Specialized DNA polymerases play a crucial role in DNA replication, particularly in tolerating persistent DNA damage.

Purpose of the Study:

  • To review the formation and repair mechanisms of non-bulky DNA lesions.
  • To provide an overview of the function of specialized DNA polymerases in translesion DNA synthesis.
  • To highlight the balance between efficiency and accuracy in specialized DNA polymerases.

Main Methods:

  • Literature review of DNA repair mechanisms.
  • Analysis of specialized DNA polymerase functions.
  • Examination of translesion DNA synthesis pathways.

Main Results:

  • Non-bulky DNA lesions are formed through various mechanisms and repaired by specific pathways.
  • Specialized DNA polymerases are essential for incorporating nucleotides opposite DNA lesions.
  • These polymerases exhibit high efficiency but low fidelity during DNA synthesis across lesions.

Conclusions:

  • Specialized DNA polymerases are critical for cell survival in the presence of DNA damage.
  • Translesion DNA synthesis, facilitated by these polymerases, allows replication to proceed past lesions.
  • Understanding these processes is key to comprehending genome stability and mutation avoidance.

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