Disruption of Ini1 leads to peri-implantation lethality and tumorigenesis in mice
Authors
Guidi, Cynthia J.Sands, Arthur T.
Zambrowicz, Brian P.
Turner, Tod K.
Demers, Delia A.
Webster, William
Smith, Thomas W.
Imbalzano, Anthony N.
Jones, Stephen N.
Student Authors
Cynthia J. GuidiDocument Type
Journal ArticlePublication Date
2001-04-21Keywords
Animals; Cell Transformation, Neoplastic; Chromosomal Proteins, Non-Histone; DNA-Binding Proteins; Embryonic and Fetal Development; *Gene Expression Regulation, Developmental; Genes, Tumor Suppressor; Mice; Mice, KnockoutCell Biology
Life Sciences
Medicine and Health Sciences
Metadata
Show full item recordAbstract
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.Source
Mol Cell Biol. 2001 May;21(10):3598-603. Link to article on publisher's siteDOI
10.1128/MCB.21.10.3598-3603.2001Permanent Link to this Item
http://hdl.handle.net/20.500.14038/33792PubMed ID
11313485Related Resources
Link to article in PubMedae974a485f413a2113503eed53cd6c53
10.1128/MCB.21.10.3598-3603.2001