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Journal of Bacteriology, August 2001, p. 4588-4598, Vol. 183, No. 15
0021-9193/01/$04.00+0   DOI: 10.1128/JB.183.15.4588-4598.2001
Copyright © 2001, American Society for Microbiology. All rights reserved.

Roles of LcrG and LcrV during Type III Targeting of Effector Yops by Yersinia enterocolitica

Kristin L. DeBord,dagger Vincent T. Lee,Dagger and Olaf Schneewind*

Department of Microbiology and Immunology, University of California Los Angeles School of Medicine, Los Angeles, California 90095

Received 1 February 2001/Accepted 27 April 2001

Yersinia enterocolitica target effector Yop proteins into the cytosol of eukaryotic cells by a mechanism requiring the type III machinery. LcrG and LcrV have been suggested to fulfill essential functions during the type III targeting of effector Yops. It is reported here that knockout mutations of lcrG caused mutant yersiniae to prematurely secrete Yops into the extracellular medium without abolishing the type III targeting mechanism (Los phenotype [loss of type III targeting specificity]). Knockout mutations in lcrV reduced type III targeting of mutant yersiniae but did not promote secretion into the extracellular medium (Not [no type III targeting]). However, knockout mutations in both genes caused Delta lcrGV yersiniae to display a Los phenotype similar to that of strains carrying knockout mutations in lcrG alone. LcrG binding to LcrV resulted in the formation of soluble LcrGV complexes in the bacterial cytoplasm. Membrane-associated, bacterial-surface-displayed or -secreted LcrG could not be detected. Most of LcrV was located in the bacterial cytoplasm; however, small amounts were secreted into the extracellular medium. These data support a model whereby LcrG may act as a negative regulator of type III targeting in the bacterial cytoplasm, an activity that is modulated by LcrG binding to LcrV. No support could be gathered for the hypothesis whereby LcrG and LcrV may act as a bacterial surface receptor for host cells, allowing effector Yop translocation across the eukaryotic plasma membrane.

* Corresponding author. Mailing address: Committee on Microbiology, Department of Molecular Genetics and Cell Biology, The University of Chicago, 920 East 58th St., Chicago, IL 60637. Phone: (773) 834-9060. Fax: (773) 702-3172. E-mail: oschnee{at}delphi.bsd.uchicago.edu.

dagger Present address: Committee on Microbiology, The University of Chicago, Chicago, IL 60637.

Dagger Present address: Department of Microbiology and Molecular Genetics, Harvard Medical School, Boston, MA 02115.

Journal of Bacteriology, August 2001, p. 4588-4598, Vol. 183, No. 15
0021-9193/01/$04.00+0   DOI: 10.1128/JB.183.15.4588-4598.2001
Copyright © 2001, American Society for Microbiology. All rights reserved.


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