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Hester P. M. Pratt

Summary. Synthesis of phospholipid during cleavage, compaction and blastocyst formation of the preimplantation mouse embryo was investigated using [methyl-3H]choline as a specific precursor. The only choline-containing lipids found to incorporate label were phosphatidylcholine and lysolecithin. [Methyl-3H]choline incorporation into lipid was detectable at the 2-cell stage and increased 9–13-fold (on a per embryo basis) during the 8-cell stage and subsequent compaction of the morula. Incorporation of choline was also elevated in the blastocyst but could not be compared accurately with the rates observed in earlier embryos due to uncertainty about the size of the endogenous choline pool at this stage. Choline kinase (assayed in vitro) was detectable at every stage, its activity increased during development and paralleled (qualitatively) the extent of phosphocholine formation in intact embryos. Phospholipid turnover and choline base exchange did not contribute significantly to [methyl-3H]choline incorporation into lipid, which is hence judged to represent denovo synthesis of phospholipid via the Kennedy pathway.

Mouse embryo lipids exhibit several features which may be characteristic of immature cells and which could influence the properties of their membranes. These include the absence of detectable sphingomyelin synthesis and the presence of demonstrable deacylation and turnover of phosphatidylcholine.

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Hester P. M. Pratt

Summary. Ovariectomy-induced delay of implantation was used to study the role of the uterine environment in controlling implantation in mice. Labelling studies in vivo showed that uterine protein synthesis and secretion is maximal 2–5 h and 24–30 h after the oestradiol injection which initiates implantation. Embryos removed from uteri 5,12 or 30 h after oestradiol injection were able to transport and utilize precursors of nucleic acids and proteins in short-term cultures at the same rate as normal embryos, although 'delayed' embryos had low levels of activity. These results suggest that 'delayed' embryos are metabolically activated within 5 h of release from delay, perhaps because of the hormonally-induced changes in uterine proteins which occur at this time.

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J. F. Bellringer, Hester P. M. Pratt and E. B. Keverne

Summary. Pregnancy block caused by exposure of mated female mice to a strange male was significantly reduced by bilateral destruction of the vomeronasal organ. Treatment of newly mated females with α-bromocriptine also produced pregnancy block. Pregnancy block also occurred in mated females exposed to strange male odours, but the blastocysts which had failed to implant were still present in the uterus and were viable for up to 15 days after mating. Implantation was induced in such mice by administration of exogenous progesterone and oestradiol.

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P. L. Kaye, G. A. Schultz, M. H. Johnson, Hester P. M. Pratt and R. B. Church

Summary. Between the 1-cell zygote and the early blastocyst stage of mouse embryos the net rate of uptake of methionine increased, the internal pool became progressively more expanded and less easily reached steady state, and the specificity of competitor amino acids changed. Sodium-dependent transport was first detected in compacted morulae (16–32-cell stage). Uptake of [14C]methylaminoisobutyric acid was detectable in blastocysts but not in unfertilized eggs. Efflux of methionine by an exchange transport system was detectable at all stages, but in intact blastocysts much higher external concentrations were required to activate exchange transport. An exchange system with properties similar to that operating at cleavage stages was exposed when blastocysts were collapsed with cytochalasin D. Since this exchange system was not detectable in isolated inner cell masses, it may be confined to the juxtacoelic surface of trophectoderm cells.

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Ruth E. Fowler, M. H. Johnson, D. E. Walters and Hester P. M. Pratt

Department of Physiology, Department of Anatomy, andtDepartment of Applied Biology, Downing Street, Cambridge, U.K.