Transposition with Tn3-family elements occurs through interaction with the host β-sliding clamp processivity factor

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.