Nucleocytoplasmic interactions in the mouse embryo.

Fertilized mammalian ova consist of haploid genomes derived from both parents and cytoplasmic components inherited largely from the female parent. These three cellular compartments must successfully interact with each other and with their environment for development to proceed. These interactions require the transposition of nuclear and cytoplasmic products between cellular compartments with resultant alteration of gene transcription and the cytoplasmic expression of preformed or newly synthesized gene products. We have investigated nuclear/ cytoplasmic interactions in the mouse embryo via the microsurgical transfer of nuclei and cytoplasm. Experiments have specifically examined the ability of nuclei from later developmental stages or from a different species to support development, volume relationships between nuclear and cytoplasmic compartments, and the nonequivalency of the maternal and paternal genomic contributions to development. The ability of egg cytoplasm to alter the function of a variety of embryonic and adult nuclei and the ability of these nuclei to support development has been extensively tested in nuclear transplantation investigations in amphibian embryos. These studies have shown that (a) early embryonic nuclei can support complete development (Briggs & King, 1952), (b) nuclei from progressively later developmental stages are less able to support development with serial transfer nuclei undergoing characteristic, clone-specific, developmental arrest (King & Briggs, 1956; Subtelny, 1965), and (c) instances of extensive but incomplete development have been achieved with differentiated adult nuclei (Gurdon, 1962; Gurdon & Uehlinger, 1966; Laskey & Gurdon, 1970; Gurdon & Laskey, 1970). The inability of differentiated nuclei to support complete development has been explained alternatively by the irreversibility of differentiation or the inability of the transplanted nuclei to revert to the rapidly dividing cleavage state without sustaining lethal chromosomal damage. Evidence for the latter is supported by cytological studies of amphibian nuclear transplant embryos (Briggs, Signoret & Humphrey, 1964; DiBerardino & Hoffner, 1970).