Cellular and genetic analysis of mouse blastocyst development

The development of mouse embryos was studied by both cellular and genetic approaches. In the cellular analysis, determination of cell fate in blastocysts and in cell populations derived from them was studied in an attempt to estimate the time that these cells become committed to their fate. In the genetic analysis, existing mutations that are lethal to mouse embryos were used to discern essential features of early development. In this review, the timing of cell determination in the inner cell mass and the primary ectoderm, and the manifestation of defects in mouse embryos that are homozygous for the A/sup y/ allele of the agouti locus were considered

<i>Chlamydia trachomatis</i> Infection of Mouse Trophoblasts

Chlamydia trachomatis (strains L2 and DE) were found to infect fertilized mouse ova in vitro. Inclusions were found in the trophoblast, but not in the embryo. </jats:p

Defective Chorioallantoic Fusion in Mid-gestation Lethality of Parthenogenone ⇔ Tetraploid Chimeras

AbstractPrevious studies of parthenogenetic embryos revealed severe perturbations of both embryonic and extraembryonic tissue lineages during postimplantation development. The majority of pure parthenogenetic concepti have no recognizable axis and exhibit preferential terminal differentiation of their trophectoderm and primitive endoderm. To further define the role of the extraembryonic lineages in parthenogenetic development, we provided them with zygote-derived extraembryonic tissues by aggregating them with fertilized tetraploid embryos. On Day 12 of combinedin vitroandin vivodevelopment, most of the embryos proper in these chimeras were entirely derived parthenogenetically, whereas their trophectoderm and primitive endoderm tissues were derived from the tetraploid component. NoIgf2expression was detected in the parthenogenetic embryo proper, indicating that imprinting was manifested in such chimeras. Typical development of the parthenogenetic embryo proper was markedly improved in comparison with pure parthenogenetic concepti, with such chimeras attaining an average of 23 somites (range, 10 to 35). However, most of the chimeras died abruptly at Day 13, and all were being resorbed at Day 14 of development. The gross normality of axial structures and organ development suggests that a major cause of failure of these chimeric parthenogenones to survive beyond mid-gestation was due to defective chorioallantoic fusion. Our results indicate that the severe perturbation of axial development seen in most pure parthenogenetic concepti is a secondary consequence of the effects of parthenogenesis on the trophectoderm and primitive endoderm lineages. Moreover, the mid-gestation death of parthenogenetic embryos proper despite the presence of zygote-derived tetraploid tissues implicates extraembryonic mesoderm in manifesting the effects of genomic imprinting