Abstract
Nuclear transfer is an effective reprogramming strategy that can redirect the utilization of nuclear instructions and ultimately phenotypes (1). When oocytes are used as the host, a somatic cell nucleus can be reprogrammed to activate the earliest stages of embryonic development (2, 3). Nuclear transfer embryos can develop until the stage when they are ready to implant into the uterus or shortly thereafter and then most degenerate. Very few nuclear transfer embryos successfully progress to term. Those that do mature are characterized by abnormalities in placentation, which in the mouse is placentomegaly (ref. 4 and Fig. 1). Recent reports, including one appearing in this issue of PNAS (5), investigate the etiology of this placentation defect in the mouse and arrive at somewhat different conclusions (5, 6).
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