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RelQ Mediates the Expression of β-Lactam Resistance in Methicillin-Resistant Staphylococcus aureus

Ajita Bhawini1, Parul Pandey2, Ashutosh Prakash Dubey2

  • 1Department of Microbiology, Institute of Medical Sciences, Banaras Hindu University, Varanasi, India.

Frontiers in Microbiology
|March 28, 2019
PubMed

Insights

Small alarmone synthetases (SASs) RelP and RelQ are crucial for beta-lactam resistance in methicillin-resistant Staphylococcus aureus (MRSA). RelQ deletion sensitizes MRSA to beta-lactams, while RelP deletion enhances resistance.

Area of Science:

  • Microbiology
  • Molecular Biology
  • Antimicrobial Resistance

Background:

  • Beta-lactam resistance in MRSA is linked to stringent response mediated by (p)ppGpp.
  • The roles of RelA-SpoT homolog (RSH) enzymes and small alarmone synthetases (SASs) in maintaining (p)ppGpp levels during beta-lactam exposure are unclear.

Purpose of the Study:

  • To investigate the contribution of two S. aureus SASs, RelP and RelQ, to beta-lactam resistance in MRSA.
  • To elucidate the mechanisms underlying the differential effects of RelP and RelQ on beta-lactam resistance.

Main Methods:

  • Gene deletion mutants (ΔrelQ, ΔrelP) of community-associated MRSA (CA-MRSA) were created.
  • Beta-lactam susceptibility testing was performed.
  • (p)ppGpp synthesis was induced using mupirocin.
  • mecA gene expression was analyzed.
  • Promoter activities of relP and relQ were compared.

Main Results:

  • Deletion of relQ significantly reduced beta-lactam resistance in CA-MRSA by impairing mecA expression.
  • Induction of (p)ppGpp synthesis bypassed the need for relQ in conferring high-level beta-lactam resistance.
  • Surprisingly, deletion of relP resulted in increased beta-lactam resistance.
  • relQ exhibits a stronger promoter activity and is induced by oxacillin, unlike relP.
  • The enhanced expression of relQ in the ΔrelP background positively impacts mecA expression, leading to higher resistance.

Conclusions:

  • RelQ plays a critical role in establishing high-level beta-lactam resistance in MRSA.
  • The interplay between RelP and RelQ, influenced by promoter strength and inducibility, determines the level of beta-lactam resistance.
  • Targeting SASs offers a potential strategy for combating MRSA infections.
Keywords:
MRSAMecARelPRelQStringent Response

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