A Brg1 null mutation in the mouse reveals functional differences among mammalian SWI/SNF complexes.

摘要: Mammalian SWI/SNF complexes utilize either brahma (Brm) or brahma-related gene 1 (Brg1) catalytic subunits to remodel nucleosomes in an ATP-dependent manner. Brm was previously shown be dispensable, suggesting that and Brg1 are functionally redundant. To test this hypothesis, we have generated a null mutation by targeting, and, surprisingly, homozygotes die during the periimplantation stage. Furthermore, blastocyst outgrowth studies indicate neither inner cell mass nor trophectoderm survives. However, experiments with other types demonstrate is not general survival factor. In addition, heterozygotes predisposed exencephaly tumors. These results provide evidence biochemically similar chromatin-remodeling dramatically different functions mammalian development.