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Related Concept Videos

Homologous Recombination02:31

Homologous Recombination

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The basic reaction of homologous recombination (HR) involves two chromatids that contain DNA sequences sharing a significant stretch of identity. One of these sequences uses a strand from another as a template to synthesize DNA in an enzyme-catalyzed reaction. The final product is a novel amalgamation of the two substrates. To ensure an accurate recombination of sequences, HR is restricted to the S and G2 phases of the cell cycle. At these stages, the DNA has been replicated already and the...
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Restarting Stalled Replication Forks02:37

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DNA replication is initiated at sites containing predefined DNA sequences known as origins of replication. DNA is unwound at these sites by the minichromosome maintenance (MCM) helicase and other factors such as Cdc45 and the associated GINS complex.The unwound single strands are protected by replication protein A (RPA) until DNA polymerase starts synthesizing DNA at the 5’ end of the strand in the same direction as the replication fork. To prevent the replication fork from falling apart,...
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Fixing Double-strand Breaks02:04

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The double-stranded structure of DNA has two major advantages. First, it serves as a safe repository of genetic information where one strand serves as the back-up in case the other strand is damaged. Second, the double-helical structure can be wrapped around proteins called histones to form nucleosomes, which can then be tightly wound to form chromosomes. This way, DNA chains up to 2 inches long can be contained within microscopic structures in a cell. A double-stranded break not only damages...
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Conservative Site-specific Recombination and Phase Variation02:53

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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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Long-patch Base Excision Repair01:02

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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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The DNA Replication Fork01:02

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An organism’s genome needs to be duplicated in an efficient and error-free manner for its growth and survival. The replication fork is a Y-shaped active region where two strands of DNA are separated and replicated continuously. The coupling of DNA unzipping and complementary strand synthesis is a characteristic feature of a replication fork.   Organisms with small circular DNA, such as E. coli, often have a single origin of replication; therefore, they have only two replication...
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Related Experiment Video

Updated: Jun 12, 2025

Detection of Homologous Recombination Intermediates via Proximity Ligation and Quantitative PCR in Saccharomyces cerevisiae
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53BP1 deficiency leads to hyperrecombination using break-induced replication (BIR).

Sameer Bikram Shah1, Youhang Li1,2, Shibo Li1,3

  • 1Department of Molecular and Cell Biology, The Scripps Research Institute, La Jolla, CA 92037, USA.

Biorxiv : the Preprint Server for Biology
|September 24, 2024
PubMed
Summary

53BP1 suppresses mutagenic break-induced replication (BIR) by preventing DNA synthesis on single-stranded DNA overhangs. Its loss triggers BIR-like hyperrecombination, offering potential cancer treatment strategies.

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Area of Science:

  • Molecular Biology
  • Genetics
  • Cancer Research

Background:

  • Break-induced replication (BIR) is a mutagenic DNA repair pathway requiring strict regulation.
  • The mechanisms controlling BIR and double-strand break (DSB) repair pathway selection are not fully understood.

Purpose of the Study:

  • To investigate the role of 53BP1 in suppressing BIR.
  • To elucidate the mechanisms of BIR regulation and DSB repair pathway choice.

Main Methods:

  • Studied the function of 53BP1 in suppressing BIR after DSB end resection.
  • Investigated the role of Polα-primase, PCNA ubiquitination, and PIF1 in BIR activation.
  • Examined the impact of SMARCAD1 on 53BP1 and BIR activation at broken replication forks.

Main Results:

  • Loss of 53BP1 induces BIR-like hyperrecombination dependent on Polα-primase.
  • 53BP1 deficiency leads to PCNA ubiquitination and PIF1 recruitment, activating BIR.
  • SMARCAD1 displaces 53BP1 at broken forks to promote BIR.
  • 53BP1 deficiency causes template switching and large deletions, increasing genome instability.

Conclusions:

  • 53BP1 plays a critical role in suppressing BIR and maintaining genome stability.
  • The interplay between 53BP1 and BIR pathways presents a synthetic lethal interaction exploitable for cancer therapy.