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Related Concept Videos

Translesion DNA Polymerases02:10

Translesion DNA Polymerases

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.
TLS polymerases are found in all three domains of life - archaea, bacteria, and eukaryotes. Of the different classes of TLS polymerases, members of the Y family are fitted with specialized structures that...
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Restarting Stalled Replication Forks

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, a...
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DNA-only Transposons

DNA-only transposons are called autonomous transposons since they code for the enzyme transposase that is required for the transposition mechanism. Insertion of transposons can alter gene functions in multiple ways. They can mutate the gene, alter gene expression by introducing a novel promoter or insulator sequence, introduce new splice sites, and change the mRNA transcripts produced, or remodel chromatin structure.
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In response to DNA damage, cells can pause the cell cycle to assess and repair the breaks. However, the cell must check the DNA at certain critical stages during the cell cycle. If the cell cycle pauses before DNA replication, the cells will contain twice the amount of DNA. On the other hand, if cells arrest after DNA replication but before mitosis, they will contain four times the normal amount of DNA. With a host of specialized proteins at their disposal,cells must use the right protein at...
DNA Damage Can Stall the Cell Cycle02:36

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Transposons make up a significant part of genomes of various organisms. Therefore, it is believed that transposition played a major evolutionary role in speciation by changing genome sizes and modifying gene expression patterns. For example, in bacteria, transposition can lead to conferring antibiotic resistance. Movement of transposable elements within the genetic pool of pathogenic bacteria can aid in transfer of antibiotic-resistant genetic elements. In eukaryotes, transposons can carry out...

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Determination of the Optimal Chromosomal Location(s) for a DNA Element in Escherichia coli Using a Novel Transposon-mediated Approach
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FtsK translocation on DNA stops at XerCD-dif.

James E Graham1, Viknesh Sivanathan, David J Sherratt

  • 1Department of Biochemistry, University of Oxford, Oxford, UK.

Nucleic Acids Research
|October 27, 2009
PubMed
Summary

Escherichia coli FtsK DNA translocase specifically stops at XerCD-dif sites, preventing protein removal and enabling chromosome unlinking. This interaction is crucial for proper cell division and genetic stability.

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Quantitation and Analysis of the Formation of HO-Endonuclease Stimulated Chromosomal Translocations by Single-Strand Annealing in Saccharomyces cerevisiae

Published on: September 23, 2011

Area of Science:

  • Molecular Biology
  • Microbiology
  • Genetics

Background:

  • Escherichia coli FtsK is a DNA translocase essential for chromosome segregation during cell division.
  • FtsK facilitates sister chromosome unlinking at the division septum, guided by KOPS sequences to the dif site.
  • At dif, FtsK activates XerCD site-specific recombination, a critical step in resolving chromosome dimers.

Purpose of the Study:

  • To investigate the mechanism by which FtsK translocation interacts with the XerCD-dif recombination complex.
  • To determine if FtsK translocation stops at XerCD-dif and the consequences of this interaction.
  • To elucidate the role of the FtsKgamma regulatory subdomain and recombination activity in this process.

Main Methods:

  • In vitro DNA translocation assays using purified FtsK protein.
  • Biochemical analysis of FtsK ATPase activity in the presence of XerCD-dif complexes.
  • Investigating FtsK-DNA binding and dissociation dynamics.

Main Results:

  • FtsK translocation specifically halts at the XerCD-dif complex.
  • This stoppage prevents the removal of XerCD recombinases from the dif site.
  • FtsK ATPase activity is reduced upon stopping at XerCD-dif, without FtsK dissociation from DNA.
  • Stoppage is independent of the FtsKgamma subdomain, DNA cleavage, or synaptic complex formation.

Conclusions:

  • FtsK translocation exhibits specific pausing at XerCD-dif recombination sites.
  • This regulated stop ensures the proper activation of XerCD recombination for chromosome unlinking.
  • The mechanism of stoppage is distinct from FtsK dissociation and does not rely on FtsKgamma or full recombination activity.