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Reveals interaction between RecBCD complex and β-clamp, suggesting role in DNA repair mechanisms.
DNA sliding clamps are central coordinators of genome replication and maintenance, yet the full binding network ("interactome") of the bacterial β-clamp remains incompletely defined. Here, we report a novel interaction between Escherichia coli β-clamp and the helicase-nuclease RecBCD complex. Using bacterial two-hybrid assays and co-immunoprecipitation, supported by fluorescence microscopy, we show that RecB associates with β-clamp. Nuclear magnetic resonance spectroscopy maps the interaction to the canonical ligand pocket of β-clamp and identifies a clamp-binding motif in RecB (residues 1018-1023, QVEMEF), whose mutation abolishes binding. Functional assays indicate that this interaction occurs upon conformational switching of RecBCD at a Chi site, and disruption of the motif reduces survival after DNA damage. We also find indications of a second binding site in the helicase domain of RecB. These findings expand the β-clamp interactome and suggest a previously unappreciated role for β-clamp in DNA double-strand break repair, with potential implications for antibacterial strategies.
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Riisnæs et al. (2026) studied this question.
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