Loss of Max function in the mouse resulted in generalized developmental arr
est of both embryonic and extraembryonic tissues at early postimplantation
(similar to E5.5-6.5), coincident with loss or dilution of maternal Max sto
res in the expanding embryo in vivo and in blastocyst outgrowths in vitro.
Developmentally arrested embryos were reduced in size and exhibited widespr
ead cytological degeneration and feeble BrdU incorporation. Max and, by ext
ension, the Myc superfamily, serve essential roles in early mammalian devel
opment and a maternal reservoir of Max exists in sufficient amount to susta
in Myc superfamily function through preimplantation stages of development.