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PubMed1978

Expression of TEM-induced damage to postmeiotic stages of spermatogenesis of the mouse during early embryogenesis. II. Cytological investigations.

After treatment of postmeiotic stages of spermatogenesis of the mouse with TEM (0.2 or 0.4 mg/kg), dose- and stage-of-spermatogenesis-dependent frequencies of cytogenetic aberrations can be observed in early embryos. The frequencies of first-cleavage metaphases exhibiting structural aberrations (all of the chromosome type), the frequencies of 2 cell embryos and of 4--8 cell embryos containing nuclei accompanied by micronuclei or nuclei connected by bridges show a close correlation to frequencies of preimplantation loss of embryos recorded in a dominant lethal test. The frequencies of morulae/blastulae exhibiting blastomeres with micronuclei show a close correlation to the frequencies of total (pre- and post-implantation) loss of embryos. This indicates delayed expression of TEM-induced chromosomal damage which could persist undetected in very early stages of embryogenesis.

Animals↗
PubMed1988

A simplified method for fixation of human and mouse preimplantation embryos which facilitates G-banding and karyotypic analysis.

A reliable method for the fixation of large numbers of preimplantation embryos was developed to allow application of routine G-banding methods to preimplantation stage embryos. The technique resulted in minimal loss of embryos and was suitable for both 1-cell mouse embryos and multi-pronuclear human embryos. Application of this method will increase the information gained from chromosome studies of embryonic development.

Animals↗
PubMedDate not supplied

[The embryotropic action of an industrial-frequency magnetic field].

The animals exposed to a magnetic field of industrial frequency with the level of induction of 250 over 4 months develop depression of their reproductive function, which fact manifests itself by decline in their potential of being able to conceive, drop in fertility because their general embryonal mortality is so high, their offspring lacking vital power, the numbers of deadborn being on the increase, their newborns dying during the first month of their life. There are also instances of female loss following delivery presenting with the events of bleeding, consequent upon disturbances in the reproductive function.

Animals↗
PubMed1973

Protein synthesis and loss of viability in rye embryos. The lability of transferase enzymes during senscence.

Poor germination and eventual loss of viability of rye grains on storage reflects a decreasing ability of embryos to synthesize protein in vivo. Cell-free protein-synthesizing systems from low viability embryo stocks exhibit lesions in the soluble components of the post-ribosomal supernatant fractions. tRNA and aminoacyl-tRNA synthetases are not impaired. The activity of enzymes concerned with transfer of phenylalanyl-tRNA from the aminoacyl to the peptidyl site on the ribosome is slightly decreased. The transfer enzymes (transferase I) involved in the binding of phenylalanyl-tRNA to the aminoacyl site show a loss of activity that closely reflects the loss of viability and the decline of protein synthesis of the embryo in vivo. The inactivation of labile transferase I components may be a major factor leading to senescence and loss of viability in rye grains.

Acyltransferases↗
PubMed2003

Blastocyst formation and cell numbers in human frozen-thawed embryos following extended culture.

BACKGROUND: Blastomere loss following human embryo cryopreservation has been shown to be associated with reduced implantation potential. In order to elucidate the underlying mechanism, the present study was designed to investigate the consequences of blastomere loss on subsequent preimplantation development in vitro. METHODS: Cryopreserved embryos destined for disposal were thawed and cultured for 96 h prior to determination of total cell numbers in resultant blastocysts. RESULTS: The proportion of embryos which formed blastocysts in vitro was significantly reduced when blastomere loss was evident in thawed embryos (25 versus 41% in fully intact thawed embryos). In addition, blastocysts from partially intact thawed embryos exhibited a significant reduction in total cell number (45.0 versus 58.4 in blastocysts from fully intact thawed embryos). Development to the blastocyst stage was significantly less frequent in fully intact thawed embryos which had been generated using ICSI (19%) compared with standard IVF (47%), although cell numbers in the resultant blastocysts were similar (57.1 and 58.6 respectively). CONCLUSIONS: Blastomere loss following cryopreservation impairs preimplantation development and results in reduced cell numbers at peri-implantation stages. ICSI is associated with reduced potential for post-thaw development of cryopreserved embryos in vitro.

Blastocyst↗
PubMed2005

Essential role of endothelial Notch1 in angiogenesis.

BACKGROUND: Notch signaling influences binary cell fate decisions in a variety of tissues. The Notch1 receptor is widely expressed during embryogenesis and is essential for embryonic development. Loss of global Notch1 function results in early embryonic lethality, but the cell type responsible for this defect is not known. Here, we identify the endothelium as the primary target tissue affected by Notch1 signaling. METHODS AND RESULTS: We generated an endothelium-specific deletion of Notch1 using Tie2Cre and conditional Notch1(flox/flox) mice. Mutant embryos lacking endothelial Notch1 died at approximately embryonic day 10.5 with profound vascular defects in placenta, yolk sac, and embryo proper, whereas heterozygous deletion had no effect. In yolk sacs of mutant embryos, endothelial cells formed a primary vascular plexus indicative of intact vasculogenesis but failed to induce the secondary vascular remodeling required to form a mature network of well-organized large and small blood vessels, which demonstrates a defect in angiogenesis. These vascular defects were also evident in the placenta, where blood vessels failed to invade the placental labyrinth, and in the embryo proper, where defective blood vessel maturation led to pericardial and intersomitic hemorrhage. Enhanced activation of caspase-3 was detected in endothelial and neural cells of mutant mice, which resulted in enhanced apoptotic degeneration of somites and the neural tube. CONCLUSIONS: These findings recapitulate the vascular phenotype of global Notch1-/- mutants and indicate an essential cell-autonomous role of Notch1 signaling in the endothelium during vascular development. These results may have important clinical implications with regard to Notch1 signaling in adult angiogenesis.

Animals↗
PubMed2003

Extra-embryonic function of Rb is essential for embryonic development and viability.

The retinoblastoma (Rb) gene was the first tumour suppressor identified. Inactivation of Rb in mice results in unscheduled cell proliferation, apoptosis and widespread developmental defects, leading to embryonic death by day 14.5 (refs 2-4). However, the actual cause of the embryonic lethality has not been fully investigated. Here we show that loss of Rb leads to excessive proliferation of trophoblast cells and a severe disruption of the normal labyrinth architecture in the placenta. This is accompanied by a decrease in vascularization and a reduction in placental transport function. We used two complementary techniques-tetraploid aggregation and conditional knockout strategies-to demonstrate that Rb-deficient embryos supplied with a wild-type placenta can be carried to term, but die soon after birth. Most of the neurological and erythroid abnormalities thought to be responsible for the embryonic lethality of Rb-null animals were virtually absent in rescued Rb-null pups. These findings identify and define a key function of Rb in extra-embryonic cell lineages that is required for embryonic development and viability, and provide a mechanism for the cell autonomous versus non-cell autonomous roles of Rb in development.

Animals↗
PubMed1993

Factors of importance for decreased early embryo survival in female mice treated neonatally with diethylstilboestrol.

Neonatal female mice of the NMRI strain were treated s.c. with 5 micrograms of the synthetic oestrogen diethylstilboestrol (DES) or vehicle only (olive oil; controls) for the first 5 days after birth. Embryos at the two-cell stage from control females were transferred to the oviducts of control females or DES-treated females (6-8-weeks-old). Immediately after transfer, the oviducts were removed and incubated in vitro for 6 h. After incubation, slightly fewer embryos were recovered from oviducts exposed to DES compared with control oviducts (81% versus 92%; 0.05 > P > 0.01). When the recovered embryos were cultured in vitro, 64% of the embryos from control oviducts reached the blastocyst stage in contrast to only 24% of those from oviducts of DES-treated mice; slightly fewer of the latter showed trophoblastic outgrowth (76% versus 93%; 0.05 > P > 0.01). Oviductal transport and uterine attachment was studied by introduction of blue-stained dextran microspheres into the oviduct. The microspheres appeared earlier in the uteri of DES-treated females than in the uteri of controls. Moreover, the spheres were not captured in the uterus in most DES-treated females, but they were trapped when a piece of Spongostan was placed in the uterine lumen. Scanning electron microscope studies showed differences between controls and DES-treated females in uterine mucosal lining of possible importance for embryo attachment to the surface epithelium. These studies showed that neonatal DES treatment caused changes in the adult reproductive tract as revealed by a detrimental effect upon embryo development, more rapid oviductal transport and loss of embryos from the uterus.

Animals↗
PubMed1982

Application of the in vitro embryo culture to the study of the mutagenic effects of nickel in male germ cells.

In vitro embryo cultures were utilized to determine the mechanism of preimplantation loss of embryos derived from matings 3 and 4 weeks after treatment of male Balb/c mice with 56 mg/kg nickel nitrate. Treated and control males were allowed to mate with superovulated females weekly for 5 weeks following treatment, and the number of cleaved eggs as well as development of embryos to blastocysts and implantation were determined. Controls included also males treated with a dose of 40 mg/kg nickel nitrate which previously had been shown to be ineffective in the dominant lethal test. Fertilizing capacity of the spermatozoa as well as development of the cultured embryos were not influenced by a dose of 40 mg/kg nickel nitrate. A dose of 56 mg/kg significantly reduced, the fertilization rate 3 and 4 weeks after treatment but did not affect development of 2-cell embryos. These results demonstrate that the preimplantation loss induced by nickel treatment of males is due to toxic effect on spermatids and spermatogonia and not to a clastogenic action.

Animals↗
PubMed2006

Roles for Dnmt3b in mammalian development: a mouse model for the ICF syndrome.

ICF (Immunodeficiency, Centromeric instability and Facial anomalies) syndrome is a rare autosomal recessive disease caused by mutations in the DNA methyltransferase gene DNMT3B. To investigate the function of Dnmt3b in mouse development and to create animal models for ICF syndrome, we have generated three mutant alleles of Dnmt3b in mice: one carrying a deletion of the catalytic domain (null allele) and two carrying ICF-like missense mutations in the catalytic domain. The Dnmt3b null allele results in embryonic lethality from E14.5 to E16.5 with multiple tissue defects, including liver hypotrophy, ventricular septal defect and haemorrhage. By contrast, mice homozygous for the ICF mutations develop to term and some survive to adulthood. These mice show phenotypes that are reminiscent of ICF patients, including hypomethylation of repetitive sequences, low body weight, distinct cranial facial anomalies and T cell death by apoptosis. These results indicate that Dnmt3b plays an essential role at different stages of mouse development, and that ICF missense mutations cause partial loss of function. These mutant mice will be useful for further elucidation of the pathogenic and molecular mechanisms underlying ICF syndrome.

Animals↗
PubMed1996

Mechanisms of reduced fertility in Hoxa-10 mutant mice: uterine homeosis and loss of maternal Hoxa-10 expression.

The establishment of a receptive uterine environment is critical for embryonic survival and implantation. One gene that is expressed in the uterus during the peri-implantation period in mice and is required for female fertility is the homeobox gene Hoxa-10. Here we characterize the peri-implantation defects in Hoxa-10 mutant females and investigate functions of Hoxa-10 in the uterine anlage during morphogenesis and in the adult uterus during pregnancy. Examination of pregnancy in Hoxa-10 mutant females has revealed failure of implantation as well as resorption of embryos in the early postimplantation period. Morphologic analysis of the mutant uterus has demonstrated homeotic transformation of the proximal 25% into oviduct. Histology and molecular markers confirm this anterior transformation. Furthermore, in situ hybridization shows that this region coincides with the anterior limit of embryonic Hoxa-10 expression in the urogenital ducts and a parallel transformation is observed in Hoxa-10 mutant males at the junction of the epididymis and ductus deferens. Female fertility could be compromised by either the homeotic transformation or the absence of Hoxa-10 function in the adult during pregnancy. To distinguish between these two potential mechanisms of infertility, wildtype blastocysts were transferred into mutant uteri distal to the transformed region on day 2.5 of pseudopregnancy. This procedure did not rescue the phenotype, suggesting that adult uterine expression of Hoxa-10 is required during pregnancy. Moreover, when implantation was experimentally delayed, homozygous uteri were able to support survival of blastocysts comparable to wild-type controls, indicating that the requirement for Hoxa-10 is intrinsic to implantation. While expression of LIF and HB-EGF appears unaffected in the mutant uteri, a decrease is observed in the intensity and number of blue dye reactions, an indicator of increased vascular permeability in response to implantation. In addition, mutant uteri exhibited decreased decidualization in response to artificial stimuli. These results show that Hoxa-10 is required during morphogenesis for proper patterning of the reproductive tract and in the adult uterus for peri-implantation events.

Animals↗
PubMed2006

Inhibiting matrix metalloproteinases with prinomastat produces abnormalities in fetal growth and development in rats.

BACKGROUND: Matrix metalloproteinases (MMPs) play key roles in remodeling of the extracellular matrix during embryogenesis and fetal development. The objective of this study was to determine the effects of prinomastat, a potent selective MMP inhibitor, on fetal growth and development. METHODS: Prinomastat (25, 100, 250 mg/kg/day, p.o.) was administered to pregnant female Sprague-Dawley rats on gestational days (GD) 6-17. A Cesarian section was carried out on GD 20 and the fetuses were evaluated for viability and skeletal and soft tissue abnormalities. RESULTS: Prinomastat treatment at the 250 mg/kg/day dose produced a decrease in body weight and food consumption in the dams. A dose-dependent increase in post-implantation loss was observed in the 100 and 250 mg/kg/day-dose groups, resulting in only 22% of the dams having viable litters for evaluation at the 250 mg/kg/day dose. Fetal skeletal tissue variations and malformations were present in all prinomastat treated groups and their frequency increased with dose. Variations and malformation in fetal soft tissue were also increased at the 100 and 250 mg/kg/day doses. Prinomastat also interfered with fetal growth of rat embryo cultures in vitro. CONCLUSIONS: These data confirm that MMP inhibition has a profound effect on fetal growth and development in vivo and in vitro.

Animals↗
PubMed2005

The role of the laminin beta subunit in laminin heterotrimer assembly and basement membrane function and development in C. elegans.

Laminins are components of basement membranes that are required for morphogenesis, organizing cell adhesions and cell signaling. Studies have suggested that laminins function as alpha(x) beta(y) gamma(z) heterotrimers in vivo. In C. elegans, there is only one laminin beta gene, suggesting that it is required for all laminin functions. Our analysis is consistent with the role of the laminin beta as a subunit of laminin heterotrimers; the same cells express the laminin alpha, beta, and gamma subunits, the laminin beta subunit localizes to all basement membranes throughout development, and secretion of the beta subunit requires an alpha subunit. RNAi inhibition of the beta subunit gene or of the other subunit genes causes an embryonic lethality phenotype. Furthermore, a distinctive set of phenotypes is caused by both viable laminin alpha and beta partial loss-of-function mutations. These results show developmental roles for the laminin beta subunit, and they provide further genetic evidence for the importance of heterotrimer assembly in vivo.

Animals↗
PubMed1992

Role of the embryonic vesicle and progesterone in embryonic loss in mares.

Characteristics of spontaneous embryonic loss in 21 mares were compared with those of 52 contemporary mares that maintained pregnancy. Embryonic losses were, in retrospect, grouped according to day of loss and length of the interovulatory interval, respectively, as follows: group 1, less than or equal to day 20 and less than or equal to 30 days (n = 10); group 2, less than or equal to day 20 and greater than 30 days (n = 3); and group 3, greater than day 20 and greater than 30 days (n = 8); ovulation was day 0. Mean diameter of the embryonic vesicle in group 1 was smaller (P less than 0.05) on days 12-18 than in the pregnancy-maintained group, but among the pregnancy-maintained group and the embryonic-loss groups, the mean individual growth rates of vesicles was similar (no significant difference). A more frequent (P less than 0.05) location of the vesicles in the uterine body on day 13 in group 1 was due to a greater proportion of small vesicles and for day 18 was due to a greater incidence of fixation failure. Luteal regression occurred at the expected time in 77% of the mares with loss sooner than day 20. Low concentration of progesterone on days 12, 15 and 18, a detected decrease in diameter of the corpus luteum on days 15 and 18, and an interovulatory interval of less than or equal to 30 days indicated that luteolysis was not prevented by the embryonic vesicle in group 1.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1999

Protective effects of garlic juice against embryotoxicity of methylmercuric chloride administered to pregnant Fischer 344 rats.

In order to investigate the beneficial effects of 0.5 or 1.0 g/kg Korean garlic juice against the embryotoxicity of 20 mg/kg methylmercury chloride (MMC, CH3HgCl), pregnant Fisher 344 rats were simultaneously orally administered on day 7 of gestation. On day 20 of gestation the dams were laparotomized under ether anesthesia, and the fetuses were removed and examined for toxicity of methylmercury. Garlic juice depressed the toxicity in terms of some parameters. In the case of simultaneous treatment with 0.1 g/kg garlic juice and MMC, rates of increase were 17.5% in maternal body weight, 13.2% and 41.9% in fetal and litters' weight respectively, and 37.0% in fetal survival rate. Decreasing rates were 10.0% in maternal death rate, and 6.9% and 31.3% in pre- and post-implantation loss respectively. Decreasing rates of mercury levels in dams were 67.2% in liver, 57.6% in brain, 47.2% in kidney, 42.1% in spleen and 40.9% in blood. As well, decreasing rates of mercury level in fetuses were 54.9% in all body burden, 55.9% in liver, 46.7% in kidney and 37% in brain, respectively. The number of fetal ossification centers were reduced by 23.8% to 58.0% following simultaneous treatment with 1.0 g/kg garlic juice. These findings indicated that garlic juice effectively inhibited the embryotoxicity of methylmercury in pregnant Fischer 344 rats.

Animals↗
PubMed2006

Adenomatous polyposis coli (APC) is required for normal development of skin and thymus.

The tumor suppressor gene Apc (adenomatous polyposis coli) is a member of the Wnt signaling pathway that is involved in development and tumorigenesis. Heterozygous knockout mice for Apc have a tumor predisposition phenotype and homozygosity leads to embryonic lethality. To understand the role of Apc in development we generated a floxed allele. These mice were mated with a strain carrying Cre recombinase under the control of the human Keratin 14 (K14) promoter, which is active in basal cells of epidermis and other stratified epithelia. Mice homozygous for the floxed allele that also carry the K14-cre transgene were viable but had stunted growth and died before weaning. Histological and immunochemical examinations revealed that K14-cre-mediated Apc loss resulted in aberrant growth in many ectodermally derived squamous epithelia, including hair follicles, teeth, and oral and corneal epithelia. In addition, squamous metaplasia was observed in various epithelial-derived tissues, including the thymus. The aberrant growth of hair follicles and other appendages as well as the thymic abnormalities in K14-cre; Apc(CKO/CKO) mice suggest the Apc gene is crucial in embryonic cells to specify epithelial cell fates in organs that require epithelial-mesenchymal interactions for their development.

Adenomatous Polyposis Coli Protein↗
PubMed1989

Maternal fertility, reproductive loss, and defective human embryos.

It is possible that many abnormal conceptuses are lost at an early stage without the mother's knowledge. To investigate this further the reproductive history of the mothers of defective embryos (neural tube defects, holoprosencephaly, cleft lip, polydactyly, and early embryonic resorption) was compared with that of the mothers of normal embryos. The frequency of prior miscarriages was higher in the case mothers than in normal controls matched for maternal age and gravidity, the difference being significant for all the anomalies except for polydactyly. The case mothers had fewer prior recognised pregnancies than control mothers matched for maternal age. There were more primigravid mothers in abnormal groups, and the difference from controls was significant for neural tube defects. It was assumed that the gravidity of the case mothers may be underestimated, possibly due to increased early abortions which are not recognised clinically. Thus, it seems that both recognised and unrecognised abortions occur more often in the mothers of defective embryos. Since many spontaneous abortuses are morphologically and/or cytogenetically abnormal, some women appear to conceive abnormal embryos repeatedly. Most of these embryos, however, may be screened out prenatally and escape clinical detection. Information on prior reproductive history of the woman should be examined carefully in genetic counselling.

Abortion, Habitual↗