DNA Repair in Staphylococcus aureus

Abstract

Staphylococcus aureus is a common cause of both superficial and invasive infections of humans and animals. Despite a potent host response and apparently appropriate antibiotic therapy, staphylococcal infections frequently become chronic or recurrent, demonstrating a remarkable ability of S. aureus to withstand the hostile host environment.

How to survive pig farming: Mechanism of SCCmec element deletion and metabolic stress adaptation in livestock-associated MRSA

“…Although actual activation of the synthesized proteins cannot be followed by transcriptional analysis, some of the genes associated with SOS response in S. aureus are transcriptionally induced, i.e., the topoisomerase IV genes par E and par C at 10 and 60 min (1.3 /0.6 and 1.7 /0.8 log2FC) after exposure to porcine serum ( Supplementary Table 2 ). The LexA-regulated low-fidelity and error-prone DNA polymerase V ( Ha and Edwards, 2021 ) umu C (1.7 log2FC) and genes involved in nucleotide excision repair ( uvr A/B; 1.5/1.2 log2FC) are significantly induced after 60 min of exposure to ammonia. Since a similar SOS-mediated induction of ccr genes by cleavage of LexA from its promoter sequence was reported previously ( Liu et al, 2017 ), the transcriptional response of both ccr variants was evaluated.…”

Microbial resistance to nanotechnologies: An important but understudied consideration using antimicrobial nanotechnologies in orthopaedic implants

“…The conversion of wild-type S. aureus to methicillin-resistant S. aureus (MRSA) is not a rare phenomenon occurring in patients with prolonged use (∼11 weeks) of antibiotics, and as a result ∼ 8.5% of such patients had experienced treatment failure post prosthetic bone/joint surgery [ 32 ]. Mechanistic investigations have found a strong correlation of staphylococcal resistance to a synergistic action of pathogenic stress response, damage repair, and self-protection [ [33] , [34] , [35] , [36] ]. Another pathway to acquire antimicrobial resistance is by forming a sessile bacterial community [ 37 ].…”

XerC is required for the repair of antibiotic- and immune-mediated DNA damage inStaphylococcus aureus

“…The main pathway used by bacteria to repair DNA damage is the SOS response, which regulates expression of genes responsible for DNA repair [Ha and Edwards, 2021]. In S. aureus , DNA double strand breaks are processed by the helicase/nuclease activity of RexAB (a member of the RecBCD/AddAB family) to generate single stranded DNA [Ha et al ., 2020].…”

“…In S. aureus , DNA double strand breaks are processed by the helicase/nuclease activity of RexAB (a member of the RecBCD/AddAB family) to generate single stranded DNA [Ha et al ., 2020]. This is then bound by RecA, forming a nucleoprotein filament that triggers the autocleavage of LexA, a transcriptional repressor, derepressing expression of genes in the SOS regulon [Ha and Edwards, 2021]. In S. aureus , the SOS regulon consists of 16 genes, including lexA and recA , and several genes involved in repairing various types of DNA damage, including nucleotide excision repair and the processing of stalled replication forks [Cirz et al ., 2007].…”

“…Unfortunately, while the SOS response has been well characterised in several model bacteria, the response of S. aureus differs significantly from these and is poorly understood. For example, the SOS regulons of E. coli and B. subtilis comprise 43 and 63, genes, respectively, many more than the 16 in S. aureus [Ha and Edwards, 2021]. Additionally, which genes are required for induction of the SOS response, and may therefore constitute good therapeutic targets, is not well understood.…”