In this section
The publication feed below is often incomplete and out of date; for an up to date summary of our publications please see Google Scholar or Pub Med
@article{Ledger:2023:10.1101/2022.09.04.506505,
author = {Ledger, E and Lau, K and Tate, E and Edwards, A},
doi = {10.1101/2022.09.04.506505},
journal = {Antimicrobial Agents and Chemotherapy},
pages = {1--11},
title = {XerC is required for the repair of antibiotic- and immune-mediated DNA damage in staphylococcus aureus},
url = {http://dx.doi.org/10.1101/2022.09.04.506505},
volume = {67},
year = {2023}
}
TY - JOUR
AB - To survive in the host environment, pathogenic bacteria need to be able to repair DNA damage caused by both antibiotics and the immune system. The SOS response is a key bacterial pathway to repair DNA double-strand breaks and may therefore be a good target for novel therapeutics to sensitize bacteria to antibiotics and the immune response. However, the genes required for the SOS response in Staphylococcus aureus have not been fully established. Therefore, we carried out a screen of mutants involved in various DNA repair pathways to understand which were required for induction of the SOS response. This led to the identification of 16 genes that may play a role in SOS response induction and, of these, 3 that affected the susceptibility of S. aureus to ciprofloxacin. Further characterization revealed that, in addition to ciprofloxacin, loss of the tyrosine recombinase XerC increased the susceptibility of S. aureus to various classes of antibiotics, as well as to host immune defenses. Therefore, the inhibition of XerC may be a viable therapeutic approach to sensitize S. aureus to both antibiotics and the immune response.
AU - Ledger,E
AU - Lau,K
AU - Tate,E
AU - Edwards,A
DO - 10.1101/2022.09.04.506505
EP - 11
PY - 2023///
SN - 0066-4804
SP - 1
TI - XerC is required for the repair of antibiotic- and immune-mediated DNA damage in staphylococcus aureus
T2 - Antimicrobial Agents and Chemotherapy
UR - http://dx.doi.org/10.1101/2022.09.04.506505
UR - https://journals.asm.org/doi/full/10.1128/aac.01206-22
UR - http://hdl.handle.net/10044/1/102135
VL - 67
ER -
Prof. Ed Tate
GSK Chair in Chemical Biology
Department of Chemistry
Molecular Sciences Research Hub, White City Campus,
82 Wood Lane, London, W12 0BZ
e.tate@imperial.ac.uk
Tel: +44 (0)20 759 + ext 43752 or 45821