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Molecular and Cellular Biology, December 2001, p. 8365-8370, Vol. 21, No. 24
0270-7306/01/$04.00+0   DOI: 10.1128/MCB.21.24.8365-8370.2001
Copyright © 2001, American Society for Microbiology. All rights reserved.

TDAG51 Is Not Essential for Fas/CD95 Regulation and Apoptosis In Vivo

Jaerang Rho,1 Shiaoching Gong,2 Nacksung Kim,1 and Yongwon Choi1,*

Department of Pathology and Laboratory Medicine, University of Pennsylvania School of Medicine, Philadelphia, Pennsylvania 19104,1 and Laboratory of Molecular Biology, The Rockefeller University, New York, New York 100212

Received 25 June 2001/Returned for modification 6 August 2001/Accepted 22 August 2001

Fas/CD95 is a key regulator of apoptotic signaling, which is crucial for the maintenance of homeostasis in peripheral lymphoid organs. TDAG51 has been shown to play critical roles in the up-regulation of Fas gene expression and T-cell apoptosis in vitro. In order to identify the role of TDAG51 in vivo, we generated TDAG51-deficient (TDAG51-/-) mice. Northern blotting revealed no expression of TDAG51 in TDAG51-/- mice, indicating that the TDAG51 gene was successfully targeted. TDAG51-/- mice were healthy and showed no gross developmental abnormalities. While Fas-deficient mice display marked lymphadenopathy, splenomegaly, and lymphocytosis, TDAG51-/- mice had no apparent defects in secondary lymphoid organs. Although TDAG51 is required for up-regulation of Fas expression in T-cell hybridomas, TDAG51-/- mice expressed normal levels of Fas and had normal T-cell apoptosis. Therefore, we conclude that TDAG51 is not essential for Fas up-regulation and T-cell apoptosis in vivo. There are several known homologs of TDAG51, and these homologs may substitute for TDAG51 in TDAG51-/- mice.

* Corresponding author. Mailing address: Abramson Family Cancer Research Institute, Department of Pathology and Laboratory Medicine, University of Pennsylvania, School of Medicine, Room 308, BRB II/III, 421 Curie Blvd., Philadelphia, PA 19104. Phone: (215) 746-6404. Fax: (215) 573-0888. E-mail: ychoi3{at}mail.med.upenn.edu.

Molecular and Cellular Biology, December 2001, p. 8365-8370, Vol. 21, No. 24
0270-7306/01/$04.00+0   DOI: 10.1128/MCB.21.24.8365-8370.2001
Copyright © 2001, American Society for Microbiology. All rights reserved.


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