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Molecular and Cellular Biology, May 2002, p. 3103-3110, Vol. 22, No. 9
0270-7306/02/$04.00+0     DOI: 10.1128/MCB.22.9.3103-3110.2002
Copyright © 2002, American Society for Microbiology. All Rights Reserved.

Tumor Suppression by a Severely Truncated Species of Retinoblastoma Protein

Hong Yang,1 Bart O. Williams,2,3,{dagger} Phillip W. Hinds,4 T. Shane Shih,2,3 Tyler Jacks,2,3,5 Roderick T. Bronson,4 and David M. Livingston1*

Dana-Farber Cancer Institute and Harvard Medical School,1 Department of Pathology, Harvard Medical School, Boston, Massachusetts 02115,4 Howard Hughes Medical Institute,5 Center for Cancer Research,2 Department of Biology, Massachusetts Institute of Technology, Cambridge, Massachusetts 021393

Received 4 June 2001/ Returned for modification 13 August 2001/ Accepted 25 January 2002

Rb+/+:Rb-/- chimeric mice are healthy until early in adulthood when they develop lethal pituitary tumors composed solely of Rb-/- cells. In an effort to delineate the minimal structures of the retinoblastoma protein necessary for RB tumor suppression function, chimeric animals derived from stably transfected RB-/- embryonic stem (ES) cells were generated. One such ES cell transfectant expressed a human RB allele encoding a stable, truncated nuclear derivative lacking residues 1 to 378 ({Delta}1-378). Others encoded either wild-type human RB or an internally deleted derivative of the {Delta}1-378 mutant. All gave rise to viable chimeric animals with comparable degrees of chimerism. However, unlike control mice derived, in part, from naive Rb-/- ES cells or from ES cells transformed by the double RB mutant, {Delta}1-378/{Delta}exon22, animals derived from either wild-type RB- or {Delta}1-378 RB-producing ES cells failed to develop pituitary tumors. Thus, in this setting, a substantial fraction of the RB sequence is unnecessary for RB-mediated tumor suppression.

* Corresponding author. Mailing address: Dana-Farber Cancer Institute and Harvard Medical School, 44 Binney St., Boston, MA 02115. Phone: (617) 632-3074. Fax: (617) 632-4381. E-mail: david_livingston{at}dfci.harvard.edu.

{dagger} Present address: Van Andel Research Institute, Grand Rapids, MI 49503.

Molecular and Cellular Biology, May 2002, p. 3103-3110, Vol. 22, No. 9
0022-538X/02/$04.00+0     DOI: 10.1128/MCB.22.9.3103-3110.2002
Copyright © 2002, American Society for Microbiology. All Rights Reserved.



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