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Overview of Transposition and Recombination02:13

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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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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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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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LTR retrotransposons are class I transposable elements with long terminal repeats flanking an internal coding region. These elements are less abundant in mammals compared to other class I transposable elements. About 8 percent of human genomic DNA comprises LTR retrotransposons. Some of the common examples of LTR retrotransposons are Ty elements in yeast and Copia elements in Drosophila.
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Translocation of proteins across membranes is an ancient process that occurs even in bacteria and archaebacteria. In fact, the components of the translocation machinery are still conserved between prokaryotes and eukaryotes.
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Transposition with Tn3-family elements occurs through interaction with the host β-sliding clamp processivity factor.

Yu Tang1, Jianfeng Zhang2,3, Jiahao Guan3

  • 1Department of Laboratory Medicine, Shanghai East Hospital, Tongji University School of Medicine, Shanghai 200123, China.

Nucleic Acids Research
|August 9, 2024
PubMed
Summary

Tn3 family transposons utilize a novel QLxxLR motif to interact with host DNA replication machinery (DnaN). This interaction is crucial for their transposition, influencing target site selection and antibiotic resistance spread.

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Area of Science:

  • Molecular Biology
  • Genetics
  • Microbiology

Background:

  • Tn3 family transposons are key drivers of antibiotic resistance dissemination.
  • The transposase (TnpA) mediates DNA breakage and rejoining for transposition.
  • Mechanisms of target site selection for these transposons are not fully understood.

Purpose of the Study:

  • To elucidate the molecular mechanism of target site selection in Tn3 family transposons.
  • To identify host factors interacting with Tn3 transposases.
  • To understand how transposons bias their integration into the host genome.

Main Methods:

  • Identification of a conserved QLxxLR motif in Tn3 transposases.
  • Biochemical assays to demonstrate interaction between Tn1721 TnpA and the host β-sliding clamp (DnaN).
  • Transposition assays to assess the role of the TnpA-DnaN interaction.

Main Results:

  • A conserved QLxxLR motif was identified in the N-terminus of Tn3 TnpAs.
  • This motif mediates interaction between Tn1721 TnpA and the host β-sliding clamp (DnaN).
  • The TnpA-DnaN interaction is essential for Tn1721 transposition, indicating a role in target site selection.

Conclusions:

  • Tn3 family transposons can bias transposition into specific replication forks via interaction with host replication machinery.
  • This interaction mechanism expands the known strategies used by mobile genetic elements to influence integration.
  • Understanding this mechanism provides insights into the spread of antibiotic resistance genes.