Disruption of Ini1 Leads to Peri-Implantation Lethality and Tumorigenesis in Mice
AUTOR(ES)
Guidi, Cynthia J.
FONTE
American Society for Microbiology
RESUMO
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.
ACESSO AO ARTIGO
http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=100281Documentos Relacionados
- Targeted Disruption of Mouse Yin Yang 1 Transcription Factor Results in Peri-Implantation Lethality
- Mcl-1 deficiency results in peri-implantation embryonic lethality
- Mitochondrial DNA Instability and Peri-Implantation Lethality Associated with Targeted Disruption of Nuclear Respiratory Factor 1 in Mice
- Peri-Implantation Lethality in Mice Lacking the Sm Motif-Containing Protein Lsm4
- Transcriptional Repression of Peri-Implantation EMX2 Expression in Mammalian Reproduction by HOXA10