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Infection and Immunity, February 1999, p. 708-716, Vol. 67, No. 2
0019-9567/99/$04.00+0
Copyright © 1999, American Society for Microbiology. All rights reserved.

YopJ of Yersinia spp. Is Sufficient To Cause Downregulation of Multiple Mitogen-Activated Protein Kinases in Eukaryotic Cells

Lance E. Palmer,1 Alessandra R. Pancetti,1,dagger Steven Greenberg,2 and James B. Bliska1,*

Department of Molecular Genetics and Microbiology, School of Medicine, State University of New York at Stony Brook, Stony Brook, New York 11794-5222,1 and Departments of Medicine and Pharmacology, Columbia University College of Physicians and Surgeons, New York, New York 100322

Received 21 July 1998/Returned for modification 24 September 1998/Accepted 3 October 1998

Pathogenic Yersinia spp. utilize a plasmid-encoded type III secretion system to deliver a set of Yop effector proteins into eukaryotic cells. Previous studies have shown that the effector YopJ is required for Yersinia to cause downregulation of the mitogen-activated protein (MAP) kinases c-Jun N-terminal kinase (JNK), p38, and extracellular signal-regulated kinase (ERK) 1 and 2 in infected macrophages. Here we demonstrate that YopJ is sufficient to cause downregulation of multiple MAP kinases in eukaryotic cells. Cellular fractionation experiments confirmed that YopJ is delivered into the cytoplasmic fraction of macrophages by the type III system. Production of YopJ in COS-1 cells by transfection significantly reduced (5- to 10-fold) activation of JNK, p38, and ERK in response to several different stimuli, including serum and tumor necrosis factor alpha. JNK activation mediated by RacV12, an activated mutant of Rac1, was also blocked by YopJ in COS-1 cells, indicating that YopJ acts downstream of this small GTPase to downregulate MAP kinase signaling. Analysis of transfected COS-1 cells by immunofluorescence microscopy revealed that YopJ is recruited from the cytoplasmic compartment to the cell periphery in response to stimuli (e.g., serum) that induce membrane ruffling. These data indicate that YopJ functions as a "MAP kinase toxin" to selectively block nuclear responses that are triggered by Yersinia-host cell interaction.

* Corresponding author. Mailing address: Department of Molecular Genetics and Microbiology, School of Medicine, State University of New York at Stony Brook, Stony Brook, NY 11794-5222. Phone: (516) 632-8782. Fax: (516) 632-9797. E-mail: bliska{at}asterix.bio.sunysb.edu.

dagger Present address: Yale University School of Medicine, Boyer Center for Molecular Medicine, Section of Microbial Pathogenesis, New Haven, CT 06536-0812.

Infection and Immunity, February 1999, p. 708-716, Vol. 67, No. 2
0019-9567/99/$04.00+0
Copyright © 1999, American Society for Microbiology. All rights reserved.


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