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Early mouse embryos express two morphological subtypes of intracisternal A-type particles, one resembling those occurring in mouse tumors (referred to as IAP) and the other apparently specific for early embryos [referred to as IAP(s)]. Using cloned fragments of IAP genes as labeled probes in dot-hybridization experiments, we detected IAP-related RNA sequences in mouse oocytes and preimplantation embryos. IAP RNA is relatively abundant in ovarian oocytes, is reduced in amount to l1/10th in the ovulated erg, and increases f100 times (from -1.3 x 103 to -1.5 x 10 molecules per embryo) between the one-cell stage and late blastocyst stage. Most of the IAP RNA consists of a single size class of about 5.4 kilobases, and a major fraction of this RNA is polyadenylylated. Quantitative considerations suggest that only a few percent of the IAP RNA in embryos are associated with particles. In two-cell embryos, the number of IAP RNA molecules is <1/10th the number of IAP(E) particles, suggesting that IAP(E) is genetically distinct from IAP and presumably represents a family of as yet unidentified retrovirus-like elements.Early mouse embryos regularly express several types of virus-like structures whose appearance is correlated with specific stages of development (for review, see refs. 1 and 2). Intracisternal A-type particles (IAPs), of which two morphological subtypes have been distinguished (3,4), are the most prominent. Particles of one subtype, termed "small A particles" (3) or, more recently, "s-particles" to emphasize their distinctness (4), seem to be specific for early embryonic cells and form in large clusters in two-to eight-cell embryos but are absent or sparse at other stages (3-7). We will refer to these particles as IAP(E)s. The other subtype, designated "large A particles" by Chase and Pik6 (3) (3,4). In this report, we will restrict the term UAP to this second type of A particle. The role of either subtype of A particle in embryo development is unclear at present, but there is evidence for the cell-surface expression of IAPrelated antigens in early embryonic cells (9, 10).The IAPs found in tumor cells have many properties resembling those of infectious retroviruses, but IAPs are genetically distinct from the mouse type B and type C viruses (11,12). IAPs have reverse transcriptase activity (13) and contain polyadenylylated RNA of 3.5 to 7 kilobases (kb) (14, 15), which codes for the major particle protein p73 (14). There are 1,000 TAP genes (provirus-like genetic elements) per haploid mouse genome (15)(16)(17), and genomic clones of several of these have been isolated and analyzed (15,18,19). The predominant gene form is 7 kb in length (18, 19), but shorter units with major deletions and substitutions also have been found (15,17). IAP genes are bordered by direct long terminal repeats (LTRs) of about 0.35 kb, which are similar in structure to the proviral LTRs of infectious retroviruses (20, 21). IAP gene insertions were found in two mutant mouse K light-chain genes (21) and in a cellular oncogene (22),...

The role of the mitochondrial genome in early development and differentiation was studied in mouse embryos cultured in vitro from the two to four cell stage to the blastocyst (about 100 cells) . During this period the mitochondria undergo morphological differentiation : progressive enlargement followed by an increase in matrix density, in number of cristae, and in number of mitochondrial ribosomes . Mitochondrial ribosomal and transfer RNA synthesis occurs from the 8 to 16 cell stage on and contributes to the establishment of a mitochondrial protein-synthesizing system . Inhibition of mitochondrial RNA-and proteinsynthesis by 0 .1 µg/ml of ethidium bromide or 31 .2 ug/ml of chloramphenicol permits essentially normal embryo development and cellular differentiation . Mitochondrial morphogenesis is also nearly normal except for the appearance of dilated and vesicular cristae in blastocyst mitochondria . Such blastocysts are capable of normal postimplantation development when transplanted into the uteri of foster mothers. Higher concentrations of these inhibitors have general toxic effects and arrest embryo development . It is concluded that mitochondrial differentiation in the early mouse embryo occurs through the progressive transformation of the preexisting mitochondria and is largely controlled by the nucleocytoplasmic system . Mitochondrial protein synthesis is required for the normal structural organization of the cristae in blastocyst mitochondria . Embryo development and cellular differentiation up to the blastocyst stage are not dependent on mitochondrial genetic activity .