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Long-patch Base Excision Repair01:02

Long-patch Base Excision Repair

Since the discovery of the two BER pathways, there has been a debate about how a cell chooses one pathway over the other and the factors determining this selection. Numerous in vitro experiments have pointed out multiple determinants for the sub-pathway selection. These are:
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Translesion (TLS) polymerases rescue stalled DNA polymerases at sites of damaged bases by replacing the replicative polymerase and installing a nucleotide across the damaged site. Doing so, TLS allows additional time for the cell to repair the damage before resuming regular DNA replication.
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Because the DNA segments are cut and reorganized in a direction-specific manner, site-specific recombination has emerged as an efficient genetic engineering technique. Flippase and Cyclization recombinases or Flp and Cre, respectively, are two members of the tyrosine recombinase family derived from bacteriophages, that are used to mediate site-specific DNA insertions, deletions, and targeted expression of proteins in mammalian cell lines.
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Quantitative Detection of DNA-Protein Crosslinks and Their Post-Translational Modifications
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Published on: April 21, 2023

Damage-specific modification of PCNA.

Sapna Das-Bradoo1, Hai Dang Nguyen, Anja-Katrin Bielinsky

  • 1University of Minnesota, Department of Biochemistry, Molecular Biology and Biophysics, Minneapolis, MN, USA.

Cell Cycle (Georgetown, Tex.)
|October 9, 2010
PubMed
Summary
This summary is machine-generated.

DNA replication involves Okazaki fragment processing. Cells signal errors in joining these fragments using ubiquitin, distinct from known repair marks, alerting replication machinery to gaps or nicks.

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Area of Science:

  • Molecular Biology
  • Cellular Biology
  • Genetics

Background:

  • Okazaki fragment processing is crucial for DNA replication, with maturation previously thought to occur post-S phase.
  • Previous studies on DNA ligase I mutants suggested Okazaki fragment maturation could be delayed.
  • Re-evaluation of DNA ligase I-deficient cells reveals new insights into lagging strand synthesis monitoring.

Purpose of the Study:

  • To investigate the cellular mechanisms for tracking lagging strand synthesis.
  • To explore the role of ubiquitin conjugation to PCNA as a cellular alarm system.
  • To discuss potential enzymatic pathways and ubiquitin attachment sites involved in signaling replication errors.

Main Methods:

  • Analysis of temperature-sensitive DNA ligase I mutants in yeast.
  • Re-evaluation of DNA ligase I-deficient cell phenotypes.
  • Investigation of ubiquitin conjugation to PCNA (Proliferating Cell Nuclear Antigen).

Main Results:

  • Failure in Okazaki fragment joining triggers a cellular alarm system involving ubiquitin conjugation to PCNA.
  • PCNA ubiquitination observed is distinct from the known post-replicative repair mark at lysine 164.
  • This modification results in both mono- and poly-ubiquitination of PCNA.

Conclusions:

  • Eukaryotic cells possess a distinct signaling pathway to detect Okazaki fragment joining errors.
  • Ubiquitin conjugation to PCNA serves as an alert for the replication machinery.
  • Different enzymatic pathways and PCNA ubiquitination sites may signal single-stranded gaps or nicks behind the replication fork.