- Keywords
- EMBRYO *, REFLEX *,
- MeSH
- Embryo, Nonmammalian * MeSH
- Embryo, Mammalian * MeSH
- Nervous System Physiological Phenomena * MeSH
- Reflex * MeSH
- Publication type
- Journal Article MeSH
After fertilization, remodeling of the oocyte and sperm genome is essential for the successful initiation of mitotic activity in the fertilized oocyte and subsequent proliferative activity of the early embryo. Despite the fact that the molecular mechanisms of cell cycle control in early mammalian embryos are in principle comparable to those in somatic cells, there are differences resulting from the specific nature of the gene totipotency of the blastomeres of early cleavage embryos. In this review, we focus on the Chk1 kinase as a key transduction factor in monitoring the integrity of DNA molecules during early embryogenesis.
- Keywords
- Chk1 kinase, DNA damage, cell cycle checkpoint, cleaving embryo,
- MeSH
- Checkpoint Kinase 1 * metabolism MeSH
- Embryo, Mammalian enzymology MeSH
- Embryonic Development * genetics MeSH
- DNA Damage * MeSH
- Animals MeSH
- Check Tag
- Animals MeSH
- Publication type
- Journal Article MeSH
- Review MeSH
- Names of Substances
- Checkpoint Kinase 1 * MeSH
OBJECTIVE: To present an overview of trials and discussion focused on the method of single embryo transfer leading to reduction of multiple pregnancy rate. SUBJECT: Review article. SETTING: Centre of Assisted Reproduction SANUS, Hradec Králové. SUBJECT AND METHOD: Transfer of two embryos after IVF results in high multiple birth (25%) associated with increased morbidity for mother and children. Results of randomized controlled trials show that SET offers live birth rate approximately 35% with minimizing the risk of twins. The trials suggest to perform SET in a group of young women (< or = 36 years old), in the first or second cycle and only with sufficient number of good quality embryos. CONCLUSIONS: Data demonstrates that a single embryo transfer strategy, currently including one fresh single embryo transfer and one addition frozen-thawed SET, results in a live birth rate comparable with double embryo transfer and significantly reduces multiple birth rate.
Carbamate pesticides generally possess low toxicity for warm-blooded vertebrates, but developmental data are scarce. We have therefore evaluated embryotoxicity of choline esterase inhibitor bendiocarbamate in the chick embryo. The pesticide was dissolved in 5% acetone in distilled water and a volume of 200 microl was administered over the embryo through membrana papyracea on embryonic days 2, 3, 4, 5, and 10. Sampling was performed on embryonic day 10, while the embryos treated on embryonic day 10 were sampled on embryonic day 17. The toxicity of bendiocarbamate was fairly low, and LD50 decreased with advancing development from 1 mg/ embryo on embryonic day 2 to 29 mg on embryonic day 5. Malformations in surviving embryos were observed rarely (< 3 %) and occurred in both control and experimental groups. There was a mild but statistically significant dose-dependent reduction in body weight, most pronounced in the treatment on embryonic days 5 and 10, but the maximum difference from controls was below 15 %. A small but not significant increase in the number of positive cells was observed in the eye, limb buds, and the central nervous system of embryos treated on embryonic days 3 and 4 and examined after supravital whole-mount staining with Lysotracker Red for apoptosis. In agreement with previously published studies in other vertebrate animals, we conclude that bendiocarbamate does not possess significant toxicity in the avian embryo.
- MeSH
- Embryo, Nonmammalian drug effects MeSH
- Carbamates toxicity MeSH
- Chick Embryo MeSH
- Pesticides toxicity MeSH
- Animals MeSH
- Check Tag
- Chick Embryo MeSH
- Animals MeSH
- Publication type
- Journal Article MeSH
- Research Support, Non-U.S. Gov't MeSH
- Names of Substances
- Carbamates MeSH
- Pesticides MeSH
To investigate the significance of impaired insulin secretion on preimplantation embryo development, outbred ICR female mice received a single injection of streptozotocin 130 mg (low) and 160 mg (subdiabetic) kg(-1), 14-17 days before fertilization. Preimplantation embryos were collected on day 3 of pregnancy, four to eight-cell embryos were cultured in vitro 48 h (day 5) and their cell number was estimated. After spontaneous ovulation, the significantly different distribution pattern in comparison with the controls was detected only in preimplantation embryos isolated from subdiabetic (160 mg x kg(-1) streptozotocin) mice. Furthermore, the incidence of degenerated embryos was significantly increased after 48 h in vitro cultivation. The analysis of cell number distribution in embryos after cultivation in vitro indicated a significant delay in cell proliferation in both experimental groups (130 and 160 mg x kg(-1) streptozotocin) in comparison with control mice. After superovulation, the only significant difference was found in the distribution pattern of embryos isolated on day 3 of pregnancy from subdiabetic (160 mg x kg(-1) streptozotocin) mice. No significant differences were found after embryo cultivation in vitro. It could be concluded that, in outbred ICR mice, lower streptozotocin treatment (130 mg x kg(-1)) influenced only cell distribution of in vitro cultured embryos after spontaneous ovulation. In ICR mice, marked changes in preimplantation embryo development were detected only after subdiabetic (160 mg x kg(-1)) streptozotocin treatment. During in vitro cultivation delayed effects of impaired insulin secretion resulted in an increase of embryo degeneration at the time after the third mitotic cleavage. Our results indicate that the effects of impaired maternal insulin secretion on preimplantation embryo development in mice are marked and consistent after spontaneous ovulation. Superovulation apparently disguises subtle changes in preimplantation embryo development after low and subdiabetic streptozotocin treatment.
- MeSH
- Time Factors MeSH
- Embryo, Mammalian anatomy & histology drug effects MeSH
- Embryonic and Fetal Development drug effects MeSH
- Embryonic Development physiology MeSH
- Mice MeSH
- Organ Culture Techniques MeSH
- Ovulation physiology MeSH
- Streptozocin pharmacology MeSH
- Superovulation MeSH
- Pregnancy MeSH
- Animals MeSH
- Check Tag
- Mice MeSH
- Pregnancy MeSH
- Female MeSH
- Animals MeSH
- Publication type
- Journal Article MeSH
- Research Support, Non-U.S. Gov't MeSH
- Names of Substances
- Streptozocin MeSH
- Keywords
- EMBRYO *,
- MeSH
- Embryo, Nonmammalian * MeSH
- Embryo, Mammalian * MeSH
- Humans MeSH
- Check Tag
- Humans MeSH
- Publication type
- Journal Article MeSH
Organisms inhabiting unpredictable environments often evolve diversified reproductive bet-hedging strategies, expressed as production of multiple offspring phenotypes, thereby avoiding complete reproductive failure. To cope with unpredictable rainfall, African annual killifish from temporary savannah pools lay drought-resistant eggs that vary widely in the duration of embryo development. We examined the sources of variability in the duration of individual embryo development, egg production and fertilization rate in Nothobranchius furzeri. Using a quantitative genetics approach (North Carolina type II design), we found support for maternal effects rather than polyandrous mating as the primary source of the variability in the duration of embryo development. The number of previously laid eggs appeared to serve as an internal physiological cue initiating a shift from rapid-to-slow embryo developmental mode. In annual killifish, extensive phenotypic variability in progeny traits is adaptive, as the conditions experienced by parents have limited relevance to the offspring generation. In contrast to genetic control, with high phenotypic expression and heritability, maternal control of traits under natural selection prevents standing genetic diversity from potentially detrimental effects of selection in fluctuating environments.
- Keywords
- diapause *, erratic rainfall *, genetic benefit *, good genes *, mating system *,
- MeSH
- Cyprinodontiformes MeSH
- Embryo, Nonmammalian MeSH
- Embryonic Development * MeSH
- Phenotype * MeSH
- Fundulidae embryology MeSH
- Adaptation, Physiological * MeSH
- Animals MeSH
- Check Tag
- Animals MeSH
- Publication type
- Journal Article MeSH
- Geographicals
- North Carolina MeSH
During the first cell-fate decision of mouse preimplantation embryo development, a population of outer-residing polar cells is segregated from a second population of inner apolar cells to form two distinct cell lineages: the trophectoderm and the inner cell mass (ICM), respectively. Historically, two models have been proposed to explain how the initial differences between these two cell populations originate and ultimately define them as the two stated early blastocyst stage cell lineages. The 'positional' model proposes that cells acquire distinct fates based on differences in their relative position within the developing embryo, while the 'polarity' model proposes that the differences driving the lineage segregation arise as a consequence of the differential inheritance of factors, which exhibit polarized subcellular localizations, upon asymmetric cell divisions. Although these two models have traditionally been considered separately, a growing body of evidence, collected over recent years, suggests the existence of a large degree of compatibility. Accordingly, the main aim of this review is to summarize the major historical and more contemporarily identified events that define the first cell-fate decision and to place them in the context of both the originally proposed positional and polarity models, thus highlighting their functional complementarity in describing distinct aspects of the developmental programme underpinning the first cell-fate decision in mouse embryogenesis.
- Keywords
- cell positioning and polarity, cell-fate, preimplantation mouse embryo,
- MeSH
- Models, Biological * MeSH
- Cell Lineage MeSH
- Embryo, Mammalian cytology physiology MeSH
- Embryonic Development physiology MeSH
- Cell Polarity * MeSH
- Signal Transduction MeSH
- Animals MeSH
- Check Tag
- Animals MeSH
- Publication type
- Journal Article MeSH
- Research Support, Non-U.S. Gov't MeSH
- Review MeSH
- Keywords
- BLOOD *, EMBRYO *,
- MeSH
- Embryo, Nonmammalian * MeSH
- Embryo, Mammalian * MeSH
- Blood * MeSH
- Blood Cells * MeSH
- Humans MeSH
- Check Tag
- Humans MeSH
- Publication type
- Journal Article MeSH
The divergence of two differentiating extraembryonic cell types (trophectoderm and primitive endoderm) from the pluripotent epiblast population (the source of fetal progenitor cells) by the blastocyst stage of mouse development relies upon the activation and execution of lineage-specific gene expression programmes. While our understanding of the central transcription factor 'effectors' directing these cell-fate choices has accumulated rapidly, what is less clear is how the differential expression of such genes within the diverging lineages is initially generated. This review summarizes and consolidates current understanding. I introduce the traditional concept and importance of a cell's spatial location within the embryo, referencing recent mechanistic and molecular insights relating to cell fate. Additionally, I address the growing body of evidence that suggests that heterogeneities among blastomeres precede, and possibly inform, their spatial segregation in the embryo. I also discuss whether the origins of such early heterogeneity are stochastic and/or indicative of intrinsic properties of the embryo. Lastly, I argue that the robustness and regulative capacity of preimplantation embryonic development may reflect the existence of multiple converging, if not wholly redundant, mechanisms that act together to generate the necessary diversity of inter-cell-lineage gene expression patterns.
- Keywords
- cell fate, preimplantation embryo, probabilistic, regulative development, stochastic, transcription,
- MeSH
- Blastomeres physiology MeSH
- Cell Differentiation physiology MeSH
- Cell Lineage physiology MeSH
- Embryo, Mammalian metabolism physiology MeSH
- Embryonic Development physiology MeSH
- Mice MeSH
- Cell Movement physiology MeSH
- Transcription Factors metabolism MeSH
- Gene Expression Regulation, Developmental physiology MeSH
- Animals MeSH
- Check Tag
- Mice MeSH
- Animals MeSH
- Publication type
- Journal Article MeSH
- Research Support, Non-U.S. Gov't MeSH
- Review MeSH
- Names of Substances
- Transcription Factors MeSH