Horizontal transfer and phylogenetic distribution of the immune evasion factor tarP
David Gerlach1,2,3, Raphael N Sieber4, Jesper Larsen4
1Interfaculty Institute of Microbiology and Infection Medicine, Infection Biology Section, University of Tübingen, Tübingen, Germany.
Abstract:
Methicillin-resistant Staphylococcus aureus (MRSA), a major human pathogen, uses the prophage-encoded tarP gene as an important immune evasion factor. TarP glycosylates wall teichoic acid (WTA) polymers, major S. aureus surface antigens, to impair WTA immunogenicity and impede host defence. However, tarP phages appear to be restricted to only a few MRSA clonal lineages, including clonal complexes (CC) 5 and 398, for unknown reasons. We demonstrate here that tarP-encoding prophages can be mobilized to lysogenize other S. aureus strains. However, transfer is largely restricted to closely related clones. Most of the non-transducible clones encode tarM, which generates a WTA glycosylation pattern distinct from that mediated by TarP. However, tarM does not interfere with infection by tarP phages. Clonal complex-specific Type I restriction-modification systems were the major reasons for resistance to tarP phage infection. Nevertheless, tarP phages were found also in unrelated S. aureus clones indicating that tarP has the potential to spread to distant clonal lineages and contribute to the evolution of new MRSA clones.
Insights
Methicillin-resistant Staphylococcus aureus (MRSA) TarP phages, crucial for immune evasion, are restricted by specific MRSA defenses. Understanding these barriers reveals potential spread to new MRSA clones.
Area of Science:
- Microbiology
- Genetics
- Immunology
Background:
- Methicillin-resistant Staphylococcus aureus (MRSA) utilizes the prophage-encoded tarP gene for immune evasion by glycosylating Wall Teichoic Acid (WTA).
- tarP phages are currently restricted to specific MRSA lineages like CC5 and CC398, with the reasons for this limitation being unclear.
Purpose of the Study:
- To investigate the mechanisms governing the host range of tarP-encoding phages in Staphylococcus aureus.
- To determine factors influencing the transfer and spread of tarP phages among different MRSA clonal lineages.
Main Methods:
- Bacteriophage transduction experiments were performed to assess the transfer of tarP-encoding prophages between various Staphylococcus aureus strains.
- Analysis of Wall Teichoic Acid (WTA) glycosylation patterns in different MRSA clones.
- Investigation of restriction-modification systems in MRSA clones resistant to tarP phage infection.
Main Results:
- tarP-encoding prophages can lysogenize other Staphylococcus aureus strains, but transfer is predominantly observed within closely related clones.
- The presence of the tarM gene in non-transducible clones does not impede tarP phage infection.
- Clonal complex-specific Type I restriction-modification systems were identified as the primary barrier to tarP phage infection in resistant MRSA clones.
Conclusions:
- Restriction-modification systems are key determinants of tarP phage host range in Staphylococcus aureus.
- Despite observed restrictions, tarP phages have the potential to spread to diverse MRSA clonal lineages, contributing to the emergence of new MRSA clones.
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