Kar Men AwNg Hien FuhCol Lin LeeThaw ZinNgeow Yun Fong2024-11-182024-11-182022-06-14https://www.microbiologyresearch.org/content/journal/jmm/10.1099/jmm.0.001547#tab2https://dspace-cris.utar.edu.my/handle/123456789/7259<jats:p>Tigecycline is an important rescue antibiotic for many bacterial infections. In <jats:italic> <jats:named-content content-type="species"> <jats:ext-link xmlns:xlink="http://www.w3.org/1999/xlink" ext-link-type="uri" xlink:href="http://doi.org/10.1601/nm.31320" xlink:type="simple">Mycobacteroides abscessus</jats:ext-link> </jats:named-content> </jats:italic>, tigecycline resistance has been associated with dysregulated stress response caused by aberrations in the interaction of the SigH and RshA factors. In this study, two tigecycline-resistant mutants of <jats:italic> <jats:named-content content-type="species"> <jats:ext-link xmlns:xlink="http://www.w3.org/1999/xlink" ext-link-type="uri" xlink:href="http://doi.org/10.1601/nm.31320" xlink:type="simple">M. abscessus</jats:ext-link> </jats:named-content> </jats:italic> (CL5A and CL6A) with mutations in the <jats:italic>rshA</jats:italic> gene were studied using gene complementation, RT-qPCR and the bacterial adenylate cyclase two-hybrid (BACTH) system. The results supported the premise that mutations in the <jats:italic>rshA</jats:italic> interrupt the RshA–SigH interaction to cause the overexpression of the <jats:italic>sigH</jats:italic> gene that leads to tigecycline resistance or reduced susceptibility.</jats:p>journal-article