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Molecular and Cellular Biology, September 2003, p. 6609-6617, Vol. 23, No. 18
0270-7306/03/$08.00+0     DOI: 10.1128/MCB.23.18.6609-6617.2003
Copyright © 2003, American Society for Microbiology. All Rights Reserved.

Apparently Normal Tumor Necrosis Factor Receptor 1 Signaling in the Absence of the Silencer of Death Domains

Robert Endres,1 Georg Häcker,1 Inge Brosch,1 and Klaus Pfeffer1,2*

Institute of Medical Microbiology, Immunology and Hygiene, Technical University of Munich, D-81675 Munich,1 Institute of Medical Microbiology, University of Düsseldorf, D-40225 Düsseldorf, Germany2

Received 17 March 2003/ Returned for modification 26 April 2003/ Accepted 16 June 2003

The silencer of death domains (SODD) has been proposed to prevent constitutive signaling of tumor necrosis factor receptor 1 (TNFR1) in the absence of ligand. Besides TNFR1, death receptor 3 (DR3), Hsp70/Hsc70, and Bcl-2 have been characterized as binding partners of SODD. In order to investigate the in vivo role of SODD, we generated mice congenitally deficient in expression of the sodd gene. No spontaneous inflammatory infiltrations were observed in any organ of these mice. Consistent with this finding, in the absence of SODD no alteration in the activation patterns of nuclear factor {kappa}B (NF-{kappa}B), stress kinases, or ERK1 or -2 was observed after stimulation with tumor necrosis factor (TNF). Activation of NF-{kappa}B by DR3 was also unchanged. The extents of DR3- and TNF-induced apoptosis were comparable in gene-deficient and wild-type cells. Protection of cells against heat shock as mediated by the Hsp70 system and against staurosporine-induced apoptosis was independent of SODD. Furthermore, resistance to high-dose lipopolysaccharide (LPS) injections, LPS-D-GalN injections, and infection with listeriae was similar in wild-type and gene-deficient mice. In conclusion, our data do not support the concept of a unique, nonredundant role of SODD for the functions of TNFR1, Hsp70, and DR3.

* Corresponding author. Mailing address: Institute of Medical Microbiology, University of Düsseldorf, Universitätsstr. 1, D-40225 Düsseldorf, Germany. Phone: 49 211 81 12459. Fax: 49 211 81 15906. E-mail: klaus.pfeffer{at}uni-duesseldorf.de.

Molecular and Cellular Biology, September 2003, p. 6609-6617, Vol. 23, No. 18
0022-538X/03/$08.00+0     DOI: 10.1128/MCB.23.18.6609-6617.2003
Copyright © 2003, American Society for Microbiology. All Rights Reserved.



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