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Molecular and Cellular Biology, July 2004, p. 6403-6409, Vol. 24, No. 14
0270-7306/04/$08.00+0     DOI: 10.1128/MCB.24.14.6403-6409.2004
Copyright © 2004, American Society for Microbiology. All Rights Reserved.

The Centrosomal, Putative Tumor Suppressor Protein TACC2 Is Dispensable for Normal Development, and Deficiency Does Not Lead to Cancer

Michael M. Schuendeln,1,{dagger} Roland P. Piekorz,1,2,{dagger},{ddagger} Christian Wichmann,1,§ Youngsoo Lee,3 Peter J. McKinnon,3 Kelli Boyd,4 Yutaka Takahashi,1,|| and James N. Ihle1,2*

Department of Biochemistry,1 Howard Hughes Medical Institute,2 Department of Genetics,3 Animal Resources Center, St. Jude Children's Research Hospital, Memphis, Tennessee 381054

Received 1 April 2004/ Accepted 27 April 2004

TACC2 is a member of the transforming acidic coiled-coil-containing protein family and is associated with the centrosome-spindle apparatus during cell cycling. In vivo, the TACC2 gene is expressed in various splice forms predominantly in postmitotic tissues, including heart, muscle, kidney, and brain. Studies of human breast cancer samples and cell lines suggest a putative role of TACC2 as a tumor suppressor protein. To analyze the physiological role of TACC2, we generated mice lacking TACC2. TACC2-deficient mice are viable, develop normally, are fertile, and lack phenotypic changes compared to wild-type mice. Furthermore, TACC2 deficiency does not lead to an increased incidence of tumor development. Finally, in TACC2-deficient embryonic fibroblasts, proliferation and cell cycle progression as well as centrosome numbers are comparable to those in wild-type cells. Therefore, TACC2 is not required, nonredundantly, for mouse development and normal cell proliferation and is not a tumor suppressor protein.

* Corresponding author. Mailing address: Department of Biochemistry, St. Jude Children's Research Hospital, 332 N. Lauderdale, Memphis, TN 38105. Phone: (901) 495-3420. Fax: (901) 525-8025. E-mail: James.Ihle{at}stjude.org.

{dagger} M.M.S. and R.P.P. contributed equally to this work.

{ddagger} Present address: Institute for Biochemistry and Molecular Biology II, Heinrich Heine University Duesseldorf, 40225 Dusseldorf, Germany.

§ Present address: Georg-Speyer-Haus, Institute for Biomedical Research, Frankfurt am Main, Germany.

|| Present address: Division of Endocrinology/Metabolism, Neurology and Hematology/Oncology, Department of Clinical Molecular Medicine, Kobe University Graduate School of Medicine, Chuo-ku, Kobe 650-0017, Japan.

Molecular and Cellular Biology, July 2004, p. 6403-6409, Vol. 24, No. 14
0022-538X/04/$08.00+0     DOI: 10.1128/MCB.24.14.6403-6409.2004
Copyright © 2004, American Society for Microbiology. All Rights Reserved.



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