The physiological functions of an increasing number of mammalian chromatin remodeling complexes have been revealed by studies of mouse mutants for the catalytic ATPase. Mutations in Brg1, Brm, Chd4, Chd2, p400 and Etl1 have been shown to be required for proper embryonic development, hematopoiesis or postnatal survival [16]–[22]. A mutant for the Snf2h, one of the two murine ISWI ATPases, revealed severe proliferation defects in the early embryo, resulting in a peri-implantation lethal phenotype [23]. Given the presence of Snf2h in multiple chromatin remodeling complexes, the assignment of biological phenotypes to different enzyme complexes can be problematic [6],[7].
