Vol:.(1234567890)
Current Microbiology (2021) 78:528–533
https://doi.org/10.1007/s00284-020-02336-1
1 3
Expressional Pattern of psm-mec System in Methicillin-Resistant
Staphylococcus aureus Under Oxacillin Stress
Deepshikha Bhowmik
1
· Shiela Chetri
1
· Piyush Pandey
1
· Bhaskar Jyoti Das
1
· Jayalaxmi Wangkheimayum
1
·
Nargis Alom Choudhury
1
· K. Melson Singha
2
· Debadatta Dhar Chanda
2
· Amitabha Bhattacharjee
1
Received: 19 May 2020 / Accepted: 14 December 2020 / Published online: 3 January 2021
© The Author(s), under exclusive licence to Springer Science+Business Media, LLC part of Springer Nature 2021
Abstract
The psm-mec element and other regulatory factors such as sarA, agrA, and RNAIII are responsible for maintaining the genetic
framework for enhanced virulence of MRSA. psm-mec is found predominantly in the staphylococcal cassette chromosome
(SCCmec). sarA, agrA, and RNAIII control gene expression to facilitate adaptation in certain environment. Genome-wide
approaches have shown that expression of virulence factors is frequently regulated at transcriptional, translational level,
and mRNA degradation level. In this study, transcriptional responses of psm-mec gene in accordance with other regulatory
factors sarA, agrA, and RNAIII were observed under normal conditions as well as when exposed to 2 μg/ml and 6 μg/ml of
oxacillin stress. One-way t-test was carried out for analysing RQ values obtained through real-time PCR. This study showed
downregulation of psm-mec gene and upregulation of other regulatory genes at lower concentration of oxacillin. However,
this was reverse when exposed against higher concentration of oxacillin. It was observed from the study that the expression
of virulence factors were dependent on each other under diferent concentration of oxacillin. Thus, this study highlights that
psm-mec, sarA, agrA, and RNAIII gene are under direct control of antibiotic pressure in a concentration-dependent manner.
Introduction
Staphylococcus aureus, a life-threatening human pathogen,
is known for its ability to produce toxins and other viru-
lence factors which can fght against the defense systems
of humans and animals. Phenol-soluble modulin (psm-
mec) is the staphylococcal cytolytic toxin that is encoded
on mobile genetic element which encodes psm-mec and
conveys methicillin-resistant S. aureus for acquisition of
antibiotic resistance and virulence determinants [1]. psm-
mec located in J2 region adjacent to mecI of the classA mec
gene complex generally disseminated among HA-MRSA.
psm-mec is also found to be encoded in Staphylococcal
Cassette Chromosome (SCCmec) type II, III, and VIII [2].
The absence or mutation of psm-mec leads to higher viru-
lence capacity of MRSA [3]. Wide varieties of virulence
factors which are responsible for the staphylococcal infec-
tion constitute a gene framework which is under the control
of global regulator—accessory gene regulator (agr). It is
also known from the other fact that agr system controls the
psm-mec gene. Though it remained unclear from the fact
that, whether psm-mec gene is under agr-dependent control
or RNAIII-independent manner [2] and also the binding of
the agrA to the psm-mec promoter is yet to be understood
[4]. In S. aureus, the expression of virulence factors are con-
trolled and coordinated by the two quorum sensing system
sar and agr. It is known that sarA protein level is important
for agr activation [5]. The agr locus acts at both transcrip-
tional and translational level, which showed increased agrA
expression, thus controlling the production of numerous
toxins, enzymes, and the cell surface proteins and regulates
the virulence factors expression [4, 6]. Functional agr regu-
latory system is essential for S. aureus virulence [4]. agr
locus consists of two divergent transcriptional loci, RNAII
and RNAIII, initiated from P2 and P3 promoters, RNAIII,
the efector molecule of agr system [5] and a second regu-
latory locus, staphylococcal accessory regulator (sar), is
Supplementary information The online version of this article
(https://doi.org/10.1007/s00284-020-02336-1) contains
supplementary material, which is available to authorized users.
* Amitabha Bhattacharjee
ab0404@gmail.com
1
Department of Microbiology, Assam University, Silchar,
Assam, India
2
Department of Microbiology, Silchar Medical College
and Hospital, Silchar, Assam, India