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Molecular and Cellular Biology, May 2001, p. 3598-3603, Vol. 21, No. 10
0270-7306/01/$04.00+0   DOI: 10.1128/MCB.21.10.3598-3603.2001
Copyright © 2001, American Society for Microbiology. All rights reserved.

Disruption of Ini1 Leads to Peri-Implantation Lethality and Tumorigenesis in Mice

Cynthia J. Guidi,1 Arthur T. Sands,2 Brian P. Zambrowicz,2 Tod K. Turner,1 Delia A. Demers,1 William Webster,3 Thomas W. Smith,4 Anthony N. Imbalzano,1 and Stephen N. Jones1,*

Departments of Cell Biology,1 Animal Medicine,3 and Pathology,4 University of Massachusetts Medical School, Worcester, Massachusetts 01655, and Lexicon Genetics, The Woodlands, Texas 773812

Received 20 December 2000/Accepted 14 February 2001

SNF5/INI1 is a component of the ATP-dependent chromatin remodeling enzyme family SWI/SNF. Germ line mutations of INI1 have been identified in children with brain and renal rhabdoid tumors, indicating that INI1 is a tumor suppressor. Here we report that disruption of Ini1 expression in mice results in early embryonic lethality. Ini1-null embryos die between 3.5 and 5.5 days postcoitum, and Ini1-null blastocysts fail to hatch, form the trophectoderm, or expand the inner cell mass when cultured in vitro. Furthermore, we report that approximately 15% of Ini1-heterozygous mice present with tumors, mostly undifferentiated or poorly differentiated sarcomas. Tumor formation is associated with a loss of heterozygocity at the Ini1 locus, characterizing Ini1 as a tumor suppressor in mice. Thus, Ini1 is essential for embryo viability and for repression of oncogenesis in the adult organism.

* Corresponding author. Mailing address: Department of Cell Biology, University of Massachusetts Medical School, 55 Lake Ave. North, Worcester, MA 01655. Phone: (508) 856-7500. Fax: (508) 856-7510. E-mail: stephen.jones{at}umassmed.edu.

Molecular and Cellular Biology, May 2001, p. 3598-3603, Vol. 21, No. 10
0270-7306/01/$04.00+0   DOI: 10.1128/MCB.21.10.3598-3603.2001
Copyright © 2001, American Society for Microbiology. All rights reserved.


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