SilE is an intrinsically disordered periplasmic ‘molecular sponge' involved in bacterial silver resistance

Asiani, Karishma R.; Williams, Huw Edward Llewelyn; Bird, Louise; Jenner, Matthew; Searle, Mark S.; Hobman, Jon L.; Scott, David J.; Soultanas, Panos

Abstract

Ag+ resistance was initially found on the Salmonella enetrica serovar Typhimurium multi-resistance plasmid pMG101 from burns patients in 1975. The putative model of Ag+ resistance, encoded by the sil operon from pMG101, involves export of Ag+ via an ATPase (SilP), an effluxer complex (SilCFBA) and a periplasmic chaperon of Ag+ (SilE). SilE is predicted to be intrinsically disordered. We tested this hypothesis using structural and biophysical studies and show that SilE is an intrinsically disordered protein in its free apo-form but folds to a compact structure upon optimal binding to six Ag+ ions in its holo-form. Sequence analyses and site-directed mutagenesis established the importance of histidine and methionine containing motifs for Ag+-binding, and identified a nucleation core that initiates Ag+-mediated folding of SilE. We conclude that SilE is a molecular sponge for absorbing metal ions.

Citation

Asiani, K. R., Williams, H. E. L., Bird, L., Jenner, M., Searle, M. S., Hobman, J. L., Scott, D. J., & Soultanas, P. (2016). SilE is an intrinsically disordered periplasmic ‘molecular sponge' involved in bacterial silver resistance. Molecular Microbiology, 101(5), 731-742. https://doi.org/10.1111/mmi.13399

• Journal Article Type: Article
• Acceptance Date: Apr 15, 2016
• Online Publication Date: May 7, 2016
• Publication Date: Aug 26, 2016
• Deposit Date: Jun 24, 2016
• Publicly Available Date: Jun 24, 2016
• Journal: Molecular Microbiology
• Print ISSN: 0950-382X
• Electronic ISSN: 1365-2958
• Publisher: Wiley
• Peer Reviewed: Peer Reviewed
• Volume: 101
• Issue: 5
• Pages: 731-742
• DOI: https://doi.org/10.1111/mmi.13399
• Public URL: https://nottingham-repository.worktribe.com/output/790929
• Publisher URL: http://onlinelibrary.wiley.com/doi/10.1111/mmi.13399/full
• Related Public URLs: http://www.ncbi.nlm.nih.gov/pubmed/27085056