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Molecular and Cellular Biology, October 2004, p. 8366-8373, Vol. 24, No. 19
0270-7306/04/$08.00+0     DOI: 10.1128/MCB.24.19.8366-8373.2004
Copyright © 2004, American Society for Microbiology. All Rights Reserved.

PAM14, a Novel MRG- and Rb-Associated Protein, Is Not Required for Development and T-Cell Function in Mice

Kaoru Tominaga,1,2* D. Mitchell Magee,3 Martin M. Matzuk,4,5,6 and Olivia M. Pereira-Smith1,2

Sam and Ann Barshop Center for Longevity and Aging Studies,1 Department of Cellular and Structural Biology,2 Department of Microbiology and Immunology, The University of Texas Health Science Center at San Antonio, San Antonio,3 Departments of Pathology,4 Molecular and Cellular Biology,5 Molecular and Human Genetics, Baylor College of Medicine, Houston, Texas6

Received 16 April 2004/ Returned for modification 28 May 2004/ Accepted 13 July 2004

PAM14 has been found to associate in complexes with the MORF4/MRG family of proteins as well as Rb, the tumor suppressor protein. This suggested that it might be involved in cell growth, immortalization, and/or senescence. To elucidate the in vivo function of PAM14, we characterized the expression pattern of mouse Pam14 and generated PAM14-deficient (Pam14–/–) mice. Pam14 was widely expressed in all mouse tissues and as early as 7 days during embryonic development. Despite this ubiquitous expression in wild-type mice, Pam14–/– mice were healthy and fertile. Response to mitogenic stimulation and production of interleukin-2 were the same in stimulated splenic T cells from Pam14–/– mice as in control littermates. Cell growth rates of mouse embryonic fibroblasts (MEFs) from all three genotypes were the same, and immortalized cells were obtained from all cell cultures during continuous culture. There was also no difference in expression of growth-related genes in response to serum stimulation in the null versus control MEFs. These data demonstrate that PAM14 is not essential for normal mouse development and cell cycle control. PAM14 likely acts as an adaptor protein in nucleoprotein complexes and is probably compensated for by another functionally redundant protein(s).

* Corresponding author. Mailing address: Sam and Ann Barshop Center for Longevity and Aging Studies, Department of Cellular and Structural Biology, The University of Texas Health Science Center at San Antonio, STCBM Bldg. 3.100, 15355 Lambda Dr., San Antonio, TX 78245-3207. Phone: (210) 562-5061. Fax: (210) 562-5093. E-mail: tominaga{at}uthscsa.edu.

Molecular and Cellular Biology, October 2004, p. 8366-8373, Vol. 24, No. 19
0022-538X/04/$08.00+0     DOI: 10.1128/MCB.24.19.8366-8373.2004
Copyright © 2004, American Society for Microbiology. All Rights Reserved.





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