There are no reports of Snf2l-null mice. However, in mice, disruption of the gene encoding the largest subunit of mammalian NURF complexes, bromodomain PHD-finger transcription factor (Bptf), is lethal to the embryo between embryonic day (E) 7.5 and E8.5 (Fig. 2). In these organisms, although the inner cell mass forms normally, the embryo does not develop a distal or anterior visceral endoderm, leading to a lack of the anteroposterior axis and primitive streak and a lack of subsequent mesodermal and endodermal differentiation56. Although BPTF-null mouse ESCs are viable, they are impaired in their ability to generate mesodermal and endodermal cell fates. BPTF also interacts with transcription factors of the SMAD family and regulates BMP-mediated signalling during the establishment of the germ layers in the embryo56. Although this is reminiscent of ISWI function in the D. melanogaster ovary8, it is unclear whether mammalian NURF complexes are similarly required for proper oogenesis. The functions of ISWI are not limited to early embryonic development in mice. Although NURF complexes function during early embryonic patterning, another SNF2L-containing complex, the CERF complex, is required later in embryogenesis: deletion of the gene encoding the CERF-specific subunit CECR2 disrupts cranium formation and causes exencephaly57.
