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Y ersinia Ysc ‐ Yop type III secretion feedback inhibition is relieved through YscV ‐dependent recognition and secretion of LcrQ
Author(s) -
Li Yunlong,
Li Lamei,
Huang Li,
Francis Matthew S.,
Hu Yangbo,
Chen Shiyun
Publication year - 2014
Publication title -
molecular microbiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.857
H-Index - 247
eISSN - 1365-2958
pISSN - 0950-382X
DOI - 10.1111/mmi.12474
Subject(s) - secretion , biology , plasmid , cytoplasm , type three secretion system , microbiology and biotechnology , virulence , activator (genetics) , biochemistry , gene
Summary Human pathogenic Y ersinia species share a virulence plasmid encoding the Ysc ‐ Yop type III secretion system ( T 3 SS ). A plasmid‐encoded anti‐activator, LcrQ , negatively regulates the expression of this secretion system. Under inducible conditions, LcrQ is secreted outside of bacterial cells and this activates the T 3 SS , but the mechanism of targeting LcrQ for type III secretion remains largely unknown. In this study, we characterized the regulatory role of the export apparatus component YscV . Depletion or overexpression of YscV compromised Yop synthesis and this primarily prevented secretion of LcrQ . It followed that a lcrQ deletion reversed the repressive effects of excessive YscV . Further characterization demonstrated that the YscV residues 493–511 located within the C ‐terminal soluble cytoplasmic domain directly bound with LcrQ . Critically, YscV ‐ LcrQ complex formation was a requirement for LcrQ secretion, since YscV Δ493–511 failed to secrete LcrQ . This forced a cytoplasmic accumulation of LcrQ , which predictably caused the feedback inhibition of Yops synthesis. Based on these observations, we proposed a model for the YscV ‐dependent secretion of LcrQ and its role in regulating Yop synthesis in Y ersinia .