A novel SigB(Q225P) mutation in Staphylococcus aureus retains virulence but promotes biofilm formation

• DOI: 10.1038/s41426-018-0078-1
• Publication Date: 2018-04-20T15:37:01Z
• Authors: Hui Liu; Weilong Shang; Zhen Hu; Ying Zheng; Jizhen Yuan; Qiwen Hu; Huagang Peng; Xinyu Cai; Li Tan; Shu Li; Junmin Zhu; Ming Li; Xiaomei Hu; Renjie Zhou; Xiancai Rao; Yi Yang
• Keywords: Virulence factor; Sigma factor; Regulon

Staphylococcus aureus is an important pathogen that produces abundant virulence factors, which cause various diseases burden human health worldwide. The stress response regulon called sigma factor B (SigB) a well-characterized global regulator involved in the regulation of S. virulence, pigmentation, and biofilm formation. However, regulatory network upon SigB incompletely described. Here, we identified novel substitution mutation, SigB(Q225P), contributed nonpigmented phenotype aureus. mutant carrying SigB(Q225P) lacks staphyloxanthin, key protecting bacteria from host-oxidant killing, but retains bacterial pathogenicity with pleiotropic alterations resulting similar lethality abscess formation ability animal models. We also reported promotion Real-time quantitative polymerase chain reaction (RT-qPCR) revealed expression nuc gene, encodes thermonuclease, was significantly downregulated, accumulation eDNA strain. LacZ reporter assay showed influenced activity promoter. Furthermore, electrophoretic mobility shift (EMSA) Bio-layer interferometry (BLI) both proteins could directly bind to gene promoter; however, binding decreased for SigB(Q225P). Our data renewed understanding relationship between golden pigment its suggested single mutation might enhance by downregulating expression.