Evolution of antimicrobial resistance in Staphylococcus aureus has been largely attributed to the horizontal transfer of mobile elements encoding anti-microbial resistance genes. Plasmid conjugation, conjugative mobilisation and transduction are the primary mechanisms of horizontal transfer in S. aureus. The ubiquitous Type I Restriction-Modification (RM) system SauI is widely believed to guide evolution of staphylococcal lineages by restricting all types of transfer between lineages. We interrogated this by testing phage infection, conjugation, mobilisation and plasmid transduction into otherwise isogenic wild-type and RM deficient mutants of several community-associated methicillin-resistant S. aureus (CA-MRSA) strains. We confirmed that the presence of a functioning RM system inhibits phage Φ11 plaque formation and plasmid transduction. However, conjugation and conjugative mobilisation were largely unaffected for representatives of the three staphylococcal conjugative families: pSK41, pWBG749 and pWBG4. The pSK41 ltrC gene conferred protection from RM systems to itself and mobilisable plasmids during conjugation and mobilisation. Protein modelling showed homology between LtrC and the known anti-restriction protein ArdC, with LtrC containing similar ssDNA-binding and metalloprotease domains as well as an additional C-terminal domain. Complementation assays showed that anti-restriction activity was re-instated when ltrC was present in the donor and recipient strains, suggesting that LtrC is involved in the process of conjugation. This work confirms that RM systems do not form an equal barrier to all forms of horizontal transfer in S. aureus, as plasmid transduction is inhibited, but conjugation and mobilisation are largely unaffected due to plasmid-encoded anti-restriction proteins.