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Avoiding self: two Tn7-encoded proteins mediate target immunity in Tn7 transposition
1Department of Molecular Biology and Genetics and the Howard Hughes Medical Institute, Johns Hopkins University School of Medicine, 725 N. Wolfe Street, Baltimore, MD 21205, USA.
The EMBO Journal
|January 10, 1998
Summary
Bacterial transposon Tn7 uses target immunity to avoid self-insertion. Proteins TnsB and TnsC act as a molecular switch, with TnsB inactivating target DNA containing Tn7 elements, preventing transposition.
Area of Science:
- Molecular Biology
- Genetics
- Biochemistry
Background:
- The bacterial transposon Tn7 possesses target immunity, preventing its transposition into DNA already containing Tn7.
- Understanding this mechanism is crucial for controlling transposon activity and gene integration.
Purpose of the Study:
- To elucidate the in vitro mechanism of Tn7 target immunity.
- To identify the roles of TnsB and TnsC proteins in this process.
Main Methods:
- In vitro biochemical assays were used to study protein-DNA interactions.
- Investigated the roles of TnsB and TnsC in binding and inactivating target DNA.
Main Results:
- TnsB (binds Tn7 ends) and TnsC (ATP-dependent DNA binding) function as a molecular switch for target immunity.
- TnsC binds target DNA, while TnsB binds and inactivates target DNA containing Tn7 ends.
- Protein-protein interactions between TnsB and TnsC, facilitated by target DNA, are key to inactivation.
- TnsB likely triggers TnsC dissociation from target DNA, dependent on ATP hydrolysis.
Conclusions:
- The TnsB-TnsC interaction model explains how Tn7 avoids self-insertion.
- This mechanism may also contribute to Tn7's preferred target site selection.