XerC belongs to the tyrosine recombinase family, which catalyzes DNA strand exchange at specific sites (dif sites) to resolve chromosomal dimers formed during replication. In R. felis, XerC likely operates in tandem with XerD, as observed in Escherichia coli and Staphylococcus aureus . Key functions include:
Genome stability: Prevention of dimer accumulation, ensuring faithful segregation during cell division.
DNA repair: Participation in the SOS response to mitigate damage from antibiotics or host immune defenses .
Mobile genetic element integration: Potential role in horizontal gene transfer, as seen in other bacteria exploiting Xer systems for plasmid/phage integration .
While recombinant R. felis XerC has not been explicitly documented, analogous systems provide insights:
Cloning strategies: Heterologous expression in E. coli using vectors like pET or pGEX, followed by affinity purification .
Enzymatic assays: Activity measured via in vitro recombination assays using synthetic dif sites or plasmid substrates .
Antibiotic resistance studies: In S. aureus, XerC deficiency increases susceptibility to fluoroquinolones and β-lactams, suggesting its role in repairing replication-associated DNA damage .
Genetic context: The xerC gene in R. felis has not been sequenced or annotated in available genomes (e.g., strain URRWXCal2) .
Regulatory interactions: Whether R. felis XerC requires FtsK-like proteins for activation, as in E. coli, remains unknown .
Pathogenesis link: Potential cross-talk between XerC-mediated DNA repair and virulence mechanisms in R. felis warrants investigation.
CRISPR/Cas9-mediated knockout: To assess XerC’s role in R. felis survival under DNA stress.
Cryo-EM studies: For structural resolution of the R. felis XerC-dif synaptic complex.
Therapeutic targeting: If XerC is essential, inhibitors could synergize with antibiotics to treat resistant infections.
KEGG: rfe:RF_1295
STRING: 315456.RF_1295