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A novel ψ-χ fusion protein for unravelling the contributions of χ to DNA replication and repair
Journal article   Peer reviewed

A novel ψ-χ fusion protein for unravelling the contributions of χ to DNA replication and repair

Kaylie A Padgett-Pagliai, Elise Wimer, Jacob D Grant, Matthew J Petrides, Elijah S P Newcomb, Vincent A Sutera, Susan T Lovett and Linda B Bloom
Nucleic acids research, Vol.54(10), 533
05/20/2026
PMID: 42200296

Abstract

Adenosine Triphosphate - metabolism DNA Polymerase III - chemistry DNA Polymerase III - genetics DNA Polymerase III - metabolism DNA Repair DNA Replication - genetics DNA-Binding Proteins - genetics DNA-Binding Proteins - metabolism Escherichia coli - genetics Escherichia coli - metabolism Escherichia coli Proteins - genetics Escherichia coli Proteins - metabolism Recombinant Fusion Proteins - chemistry Recombinant Fusion Proteins - genetics Recombinant Fusion Proteins - metabolism Zidovudine - pharmacology
Faithful DNA replication in Escherichia coli requires the DNA polymerase III holoenzyme (DNA pol III HE) and its clamp loader complex, which couples processive DNA synthesis with β-clamp loading. The clamp loader accessory subunits χ and ψ link single-stranded DNA-binding protein (SSB) to the replisome, stabilizing replication on SSB-coated templates through interactions with the SSB C-terminal tail. Chi has also been implicated in tolerance to the chain-terminating nucleoside analog azidothymidine (AZT), though whether this function depends on χ within DNA pol III HE or on its independent interaction with the YoaA helicase remains unclear. To address this, we engineered ψ-χ fusion proteins with flexible glycine-serine linkers to tether the two subunits while preserving folding and activity. Both fusions were biochemically competent, supporting ATP hydrolysis and clamp loading on SSB-coated DNA. In vivo, however, neither the ψ-GS12-χ fusion nor expression of a ψχ operon restored AZT tolerance in ΔholC cells, whereas expression of χ alone was sufficient. Fusion expression impaired growth in both wild-type (WT) and ΔholC backgrounds, a phenotype alleviated by disrupting χ-SSB binding. These findings support a model in which χ must dynamically engage SSB and YoaA outside of the clamp loader to promote AZT tolerance, highlighting the importance of regulated χ-SSB interactions in genome maintenance.
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https://doi.org/10.1093/nar/gkag533View
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