Structural highlights
Publication Abstract from PubMed
Bacteria are under constant assault by bacteriophages and other mobile genetic elements. As a result, bacteria have evolved a multitude of systems that protect from attack. Genes encoding bacterial defence mechanisms can be clustered into 'defence islands', providing a potentially synergistic level of protection against a wider range of assailants. However, there is a comparative paucity of information on how expression of these defence systems is controlled. Here, we functionally characterize a transcriptional regulator, BrxR, encoded within a recently described phage defence island from a multidrug resistant plasmid of the emerging pathogen Escherichia fergusonii. Using a combination of reporters and electrophoretic mobility shift assays, we discovered that BrxR acts as a repressor. We present the structure of BrxR to 2.15 A, the first structure of this family of transcription factors, and pinpoint a likely binding site for ligands within the WYL-domain. Bioinformatic analyses demonstrated that BrxR-family homologues are widespread amongst bacteria. About half (48%) of identified BrxR homologues were co-localized with a diverse array of known phage defence systems, either alone or clustered into defence islands. BrxR is a novel regulator that reveals a common mechanism for controlling the expression of the bacterial phage defence arsenal.
A widespread family of WYL-domain transcriptional regulators co-localizes with diverse phage defence systems and islands.,Picton DM, Harling-Lee JD, Duffner SJ, Went SC, Morgan RD, Hinton JCD, Blower TR Nucleic Acids Res. 2022 May 20;50(9):5191-5207. doi: 10.1093/nar/gkac334. PMID:35544231[1]
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine.
References
- ↑ Picton DM, Harling-Lee JD, Duffner SJ, Went SC, Morgan RD, Hinton JCD, Blower TR. A widespread family of WYL-domain transcriptional regulators co-localizes with diverse phage defence systems and islands. Nucleic Acids Res. 2022 May 20;50(9):5191-5207. doi: 10.1093/nar/gkac334. PMID:35544231 doi:http://dx.doi.org/10.1093/nar/gkac334