RelQ Mediates the Expression of β-Lactam Resistance in Methicillin-Resistant Staphylococcus aureus
An induced stringent response, which is established by an increased level of (p)ppGpp, is required for the expression of β-lactam resistance in methicillin-resistant (MRSA). However, it is not clear whether RSH (enzyme mediating stringent response to amino acid starvation) or small alarmone syntheta...
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| Published in: | Frontiers in microbiology Vol. 10; p. 339 |
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| Main Authors: | , , , , , |
| Format: | Journal Article |
| Language: | English |
| Published: |
Switzerland
Frontiers Media S.A
11-03-2019
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| Subjects: | |
| Online Access: | Get full text |
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| Summary: | An induced stringent response, which is established by an increased level of (p)ppGpp, is required for the expression of β-lactam resistance in methicillin-resistant
(MRSA). However, it is not clear whether RSH (enzyme mediating stringent response to amino acid starvation) or small alarmone synthetases (SASs) are involved in the maintenance of (p)ppGpp level in response to β-lactams. Since the
genome encodes two active SASs (RelP and RelQ), their contribution to the expression of β-lactam resistance in MRSA was investigated. It was determined that
deletion renders community-associated MRSA (CA-MRSA) sensitive to β-lactams by negatively affecting the expression of
, and induction of (p)ppGpp synthesis by mupirocin bypasses the requirement of
for the expression of high-level β-lactam resistance. Surprisingly,
deletion increased the level of β-lactam resistance. Such contradictory observations could be attributed to the fact that
promoter is ~5-fold stronger than the
and is induced by oxacillin as well as deletion of either of the SASs, while
promoter responds only to oxacillin. The stronger promoter activity of
, coupled with the inducibility of the
promoter in response to the lack of
, results in efficient expression of
in the
-deleted background. This positively affects
expression and renders the Δ
strain highly resistant. These findings indicate an important role for RelQ in the expression of high-level β-lactam resistance in MRSA. |
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| Bibliography: | ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 23 Reviewed by: Daniel Haeusser, Canisius College, United States; Shauna McGillivray, Texas Christian University, United States This article was submitted to Microbial Physiology and Metabolism, a section of the journal Frontiers in Microbiology Edited by: Kenneth C. Keiler, Pennsylvania State University, United States |
| ISSN: | 1664-302X 1664-302X |
| DOI: | 10.3389/fmicb.2019.00339 |