Staphylococcus aureus is an important human pathogen that causes a wide variety of life-threatening infections ranging from minor skin and oral infections to severe infections, such as bacteremia, pneumonia, osteomyelitis, or endocarditis due to the presence and secretion of a large number of virulence factors that are controlled by global virulence regulators in complex networks. Furthermore, S. aureus infections have become a threat to public health because of their high potential to form biofilm, and their ability to resist a wide range of antibiotics has exacerbated further. Therefore, understanding the regulatory networks and developing a drug targeting these networks has the potential to stand as therapeutic targets for future treatment of antibiotic resistant infections.
In a previous study msaC was identified as the modulator of sarA, a new global virulence regulator that controls the expression of sarA and biofilm development. Furthermore, it has also been shown that msaC is a part of four-gene operon, msaABCR operon, which includes four-genes: SAUSA300_1296 (msaA), SAUSA300_1295 (msaB), SAUSA300_1294 (msaC), and antisense RNA, msaR. The mechanism of regulation of msaABCR operon and the function of individual genes were not clearly known yet. This study defines the role of msaB, the second gene of the msaABCR operon, which will help shed some light on the regulation of msaABCR. We deleted msaB gene from USA300_LAC, and studied the major msaB phenotypes: pigmentation, protease production, biofilm formation, and rate of cell death. Deletion of msaB resulted in the similar msaC and/or msaABCR deletion mutant, thus showing the importance of this gene in this operon. The mutant showed decreased pigmentation, increased extracellular protease production, decreased biofilm formation, and increased rate of cell death. Deletion of the msaB gene also resulted in the decreased expression of some key regulators, like sarA and agr that play major roles in the regulation of virulence and biofilm formation in S. aureus, similar to msaC and msaABCR operon deletion mutant.
Thus, this study identifies the role of msaB, in the msaABCR operon, that will help us define the mechanism of regulation of virulence and biofilm formation by the msaABCR operon and provides a step to investigate the stimulatory signals that the msaABCR operon responds to during pathogenesis.
","abstract_html":"<p><em>Staphylococcus aureus</em> is an important human pathogen that causes a wide variety of life-threatening infections ranging from minor skin and oral infections to severe infections, such as bacteremia, pneumonia, osteomyelitis, or endocarditis due to the presence and secretion of a large number of virulence factors that are controlled by global virulence regulators in complex networks. Furthermore, <em>S. aureus</em> infections have become a threat to public health because of their high potential to form biofilm, and their ability to resist a wide range of antibiotics has exacerbated further. Therefore, understanding the regulatory networks and developing a drug targeting these networks has the potential to stand as therapeutic targets for future treatment of antibiotic resistant infections.</p> <p>In a previous study <em>msaC</em> was identified as the modulator of <em>sarA</em>, a new global virulence regulator that controls the expression of <em>sarA</em> and biofilm development. Furthermore, it has also been shown that <em>msaC</em> is a part of four-gene operon, <em>msaABCR</em> operon, which includes four-genes: SAUSA300_1296 (<em>msaA</em>), SAUSA300_1295 (<em>msaB</em>), SAUSA300_1294 (<em>msaC</em>), and antisense RNA, <em>msaR</em>. The mechanism of regulation of <em>msaABCR</em> operon and the function of individual genes were not clearly known yet. This study defines the role of <em>msaB</em>, the second gene of the <em>msaABCR</em> operon, which will help shed some light on the regulation of <em>msaABCR</em>. We deleted <em>msaB</em> gene from USA300_LAC, and studied the major <em>msaB</em> phenotypes: pigmentation, protease production, biofilm formation, and rate of cell death. Deletion of <em>msaB</em> resulted in the similar <em>msaC</em> and/or <em>msaABCR</em> deletion mutant, thus showing the importance of this gene in this operon. The mutant showed decreased pigmentation, increased extracellular protease production, decreased biofilm formation, and increased rate of cell death. Deletion of the <em>msaB</em> gene also resulted in the decreased expression of some key regulators, like <em>sarA</em> and <em>agr</em> that play major roles in the regulation of virulence and biofilm formation in <em>S. aureus</em>, similar to <em>msaC</em> and <em>msaABCR</em> operon deletion mutant.</p> <p>Thus, this study identifies the role of <em>msaB</em>, in the <em>msaABCR</em> operon, that will help us define the mechanism of regulation of virulence and biofilm formation by the <em>msaABCR</em> operon and provides a step to investigate the stimulatory signals that the <em>msaABCR</em> operon responds to during pathogenesis.</p>","abstract_has_math":false,"creators":["Elbarasi, Amelsaad"],"institution":null,"degree_name":"Master of Science (MS)","degree_level":"Masters Thesis","degree_discipline":"Biological Sciences","degree_department":null,"school":null,"contributors":["Mohamed O. Elasri","Glenmore Shearer","Shahid Karim"],"advisors":[],"committee_chairs":[],"committee_members":[],"year":2014,"date_issued":"2014-08-01T07:00:00Z","date_published":"2014-08-01T07:00:00Z","updated_at":"2026-07-24T05:44:27Z","subjects":["biofilm","Staphylococcus aureus","msaB gene","virulence factors","msaABCR operon","Biology","Cell and Developmental Biology","Cell Biology"],"languages":[],"rights":[],"rights_urls":[],"identifier_entries":[]},"links":{"outbound_url":"https://aquila.usm.edu/masters_theses/49","outbound_label":"Repository record","outbound_source":"dc:identifier"},"metadata_groups":[{"id":"people","label":"People","entries":[{"key":"dc:contributor","label":"Contributor","values":["Mohamed O. 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Furthermore, S. aureus infections have become a threat to public health because of their high potential to form biofilm, and their ability to resist a wide range of antibiotics has exacerbated further. Therefore, understanding the regulatory networks and developing a drug targeting these networks has the potential to stand as therapeutic targets for future treatment of antibiotic resistant infections.
In a previous study msaC was identified as the modulator of sarA, a new global virulence regulator that controls the expression of sarA and biofilm development. Furthermore, it has also been shown that msaC is a part of four-gene operon, msaABCR operon, which includes four-genes: SAUSA300_1296 (msaA), SAUSA300_1295 (msaB), SAUSA300_1294 (msaC), and antisense RNA, msaR. The mechanism of regulation of msaABCR operon and the function of individual genes were not clearly known yet. This study defines the role of msaB, the second gene of the msaABCR operon, which will help shed some light on the regulation of msaABCR. We deleted msaB gene from USA300_LAC, and studied the major msaB phenotypes: pigmentation, protease production, biofilm formation, and rate of cell death. Deletion of msaB resulted in the similar msaC and/or msaABCR deletion mutant, thus showing the importance of this gene in this operon. The mutant showed decreased pigmentation, increased extracellular protease production, decreased biofilm formation, and increased rate of cell death. Deletion of the msaB gene also resulted in the decreased expression of some key regulators, like sarA and agr that play major roles in the regulation of virulence and biofilm formation in S. aureus, similar to msaC and msaABCR operon deletion mutant.
Thus, this study identifies the role of msaB, in the msaABCR operon, that will help us define the mechanism of regulation of virulence and biofilm formation by the msaABCR operon and provides a step to investigate the stimulatory signals that the msaABCR operon responds to during pathogenesis.
"]},{"key":"dc:title","label":"Title","values":["Identification and Characterization of msaB Gene Involved in Biofilm Formation and Virulence in Staphylococcus aureus"]}]}],"canonical_facts":{"dc:contributor":["Mohamed O. Elasri","Glenmore Shearer","Shahid Karim"],"dc:creator":["Elbarasi, Amelsaad"],"dc:date.available":["2014-08-01T07:00:00Z"],"dc:description.abstract":["Staphylococcus aureus is an important human pathogen that causes a wide variety of life-threatening infections ranging from minor skin and oral infections to severe infections, such as bacteremia, pneumonia, osteomyelitis, or endocarditis due to the presence and secretion of a large number of virulence factors that are controlled by global virulence regulators in complex networks. Furthermore, S. aureus infections have become a threat to public health because of their high potential to form biofilm, and their ability to resist a wide range of antibiotics has exacerbated further. Therefore, understanding the regulatory networks and developing a drug targeting these networks has the potential to stand as therapeutic targets for future treatment of antibiotic resistant infections.
In a previous study msaC was identified as the modulator of sarA, a new global virulence regulator that controls the expression of sarA and biofilm development. Furthermore, it has also been shown that msaC is a part of four-gene operon, msaABCR operon, which includes four-genes: SAUSA300_1296 (msaA), SAUSA300_1295 (msaB), SAUSA300_1294 (msaC), and antisense RNA, msaR. The mechanism of regulation of msaABCR operon and the function of individual genes were not clearly known yet. This study defines the role of msaB, the second gene of the msaABCR operon, which will help shed some light on the regulation of msaABCR. We deleted msaB gene from USA300_LAC, and studied the major msaB phenotypes: pigmentation, protease production, biofilm formation, and rate of cell death. Deletion of msaB resulted in the similar msaC and/or msaABCR deletion mutant, thus showing the importance of this gene in this operon. The mutant showed decreased pigmentation, increased extracellular protease production, decreased biofilm formation, and increased rate of cell death. Deletion of the msaB gene also resulted in the decreased expression of some key regulators, like sarA and agr that play major roles in the regulation of virulence and biofilm formation in S. aureus, similar to msaC and msaABCR operon deletion mutant.
Thus, this study identifies the role of msaB, in the msaABCR operon, that will help us define the mechanism of regulation of virulence and biofilm formation by the msaABCR operon and provides a step to investigate the stimulatory signals that the msaABCR operon responds to during pathogenesis.
"],"dc:identifier":["https://aquila.usm.edu/masters_theses/49"],"dc:subject":["biofilm","Staphylococcus aureus","msaB gene","virulence factors","msaABCR operon","Biology","Cell and Developmental Biology","Cell Biology"],"dc:title":["Identification and Characterization of msaB Gene Involved in Biofilm Formation and Virulence in Staphylococcus aureus"],"thesis:degree_discipline":["Biological Sciences"],"thesis:degree_level":["Masters Thesis"],"thesis:degree_name":["Master of Science (MS)"]},"updated_at":"2026-07-24T05:44:27Z"}