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The centrosomal, putative tumor suppressor protein TACC2 is dispensable for normal development, and deficiency does
Michael M Schuendeln1, Roland P Piekorz, Christian Wichmann
1Department of Biochemistry, St. Jude Children's Research Hospital, Memphis, TN 38105, USA.
Abstract:
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.
Insights
Transforming acidic coiled-coil-containing protein 2 (TACC2) is not essential for mouse development or normal cell proliferation. TACC2 deficiency did not increase tumor incidence, indicating it is not a tumor suppressor protein.
Area of Science:
- Molecular Biology
- Genetics
- Developmental Biology
Background:
- Transforming acidic coiled-coil-containing protein 2 (TACC2) is a protein family member linked to the centrosome-spindle apparatus during cell division.
- TACC2 gene expression is observed in various splice forms, primarily in postmitotic tissues like the heart, muscle, kidney, and brain.
- Previous research suggested TACC2 might function as a tumor suppressor protein in human breast cancer.
Purpose of the Study:
- To investigate the physiological role of TACC2 in vivo.
- To determine if TACC2 is essential for normal mouse development and cell proliferation.
- To assess the potential tumor suppressor function of TACC2.
Main Methods:
- Generation of TACC2-deficient mice.
- Phenotypic analysis of TACC2-deficient mice compared to wild-type controls.
- Assessment of proliferation, cell cycle progression, and centrosome numbers in TACC2-deficient embryonic fibroblasts.
Main Results:
- TACC2-deficient mice were viable, developed normally, and were fertile without apparent phenotypic changes.
- No increased incidence of tumor development was observed in TACC2-deficient mice.
- TACC2-deficient embryonic fibroblasts exhibited proliferation, cell cycle progression, and centrosome numbers comparable to wild-type cells.
Conclusions:
- TACC2 is not required for normal mouse development and fertility.
- TACC2 does not play a nonredundant role in maintaining normal cell proliferation.
- The study concludes that TACC2 is not a tumor suppressor protein.
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