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Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)
 

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Disruption of Ini1 leads to peri-implantation lethality and tumorigenesis in mice.

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.[1]

References

  1. Disruption of Ini1 leads to peri-implantation lethality and tumorigenesis in mice. Guidi, C.J., Sands, A.T., Zambrowicz, B.P., Turner, T.K., Demers, D.A., Webster, W., Smith, T.W., Imbalzano, A.N., Jones, S.N. Mol. Cell. Biol. (2001) [Pubmed]
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