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PubMed1994

Sexual differentiation and preimplantation cell growth.

Growth rates of human preimplantation embryos fertilized in vitro were assessed and compared to the sex of the pregnancy outcome. The likelihood of a liveborn male was significantly greater than that of a female if the mean number of cells/embryo was four or greater at the scheduled time of transfer (odds ratio of 6:1). This finding suggested that the Y chromosome expresses factors which influence embryonic growth rates immediately after fertilization.

Blastocyst↗
PubMed1995

Autonomous proliferation of neural precursors in the tadpole retina revealed after partial removal of the embryonic eyebud.

The cellular mechanisms that regulate cell division in the developing vertebrate nervous system are essentially unknown. Using the frog retina as a model system, we tested the hypothesis that proliferation is regulated by feedback signals that encode the total number of cells in the population. To alter the number of cells in the retina, we surgically removed approximately half of the embryonic eyebud. In a previous study, cell counts made immediately after partial ablation showed that the number of proliferating, undifferentiated cells was reduced to 70% of the number in the contralateral control eye, while the number of postmitotic, differentiated cells was reduced to 47%. In this study, we sought to determine whether these reduced cell number of affected proliferation, which was assessed by counting the total number of cells present at various times after surgery. The partially ablated retinas consistently had fewer cells than the contralateral retinas. Analyses of the cell numbers suggested that there was little or no change in mitotic rate in the partially ablated retinas and that the decreased production of both differentiated and undifferentiated cells was due almost entirely to the reduction in the number of dividing cells. There is thus no evidence that retinal stem cells up-regulate their production of new cells in response to a reduction of either the stem cells themselves or of their descendants. This lack of response to population size indicates that, in contrast to many non-neural stem cell systems, proliferation of neural stem cells is not regulated by a feedback mechanism but instead is largely autonomous.

Animals↗
PubMed1991

Cyclin B mRNA depletion only transiently inhibits the Xenopus embryonic cell cycle.

The control of the cell cycle is dependent on the ability to synthesize and degrade proteins called cyclins. When antisense oligonucleotides are used to deplete Xenopus embryos of mRNA encoding cyclin B protein, embryonic cleavage is inhibited. Surprisingly, after missing several rounds of cleavage, the cell cycle and cell division resumes. These studies indicate that the early embryonic cell cycle can proceed with undetectable levels of cyclin B encoding mRNA. In contrast, other events of normal development, including the activation of embryonic transcription and gastrulation, are inhibited.

Animals↗
PubMed1997

The molecular basis of embryonic kidney development.

The development of the mature mammalian kidney begins with the invasion of metanephric mesenchyme by ureteric bud. Mesenchymal cells near the bud become induced and convert to an epithelium which goes on to generate the functional filtering unit of the kidney, the nephron. The collecting duct system is elaborated by the branching ureter, the growth of which is dependent upon signals from the metanephric mesenchyme. The process of reciprocal induction between ureter and mesenchyme is repeated many times over during development and is the key step in generating the overall architecture of the kidney. Genetic studies in mice have allowed researchers to begin to unravel the molecular signals that govern these early events. These experiments have revealed that a number of essential gene products are required for distinct steps in kidney organogenesis. Here we review and summarize the developmental role played by some of these molecules, especially certain transcription factors and growth factors and their receptors. Although the factors involved are far from completely known a rough framework of a molecular cascade which governs embryonic kidney development is beginning to emerge.

Animals↗
PubMed2004

Expression of Dbx1, Neurogenin 2, Semaphorin 5A, Cadherin 8, and Emx1 distinguish ventral and lateral pallial histogenetic divisions in the developing mouse claustroamygdaloid complex.

We studied the lateral and ventral pallial divisions of the claustroamygdaloid complex by means of analysis of expression patterns of the developmental regulatory genes Tbr1, Dbx1, Neurogenin 2, Emx1, Cadherin 8, and Semaphorin 5A in mouse developing telencephalon, from embryonic day 12.5 until birth. Our results indicate that these genes help to distinguish distinct lateral and ventral pallial histogenetic divisions in the embryonic telencephalon. Tbr1 is broadly expressed in both lateral and ventral pallial histogenetic divisions (the lateroventral migratory stream plus the mantle) during early and intermediate embryonic development; its signal becomes weak in parts of the mantle during late embryonic development. Dbx1 is strongly and specifically expressed in progenitor cells (ventricular zone) of the ventral pallium during early embryonic development, but there is no signal of this gene in the rest of the pallium nor the subpallium. Neurogenin 2 and Semaphorin 5A are both expressed in a ventral subdivision of the lateroventral migratory stream (called by us the ventral migratory stream). Further, specific nuclei of the claustral complex and pallial amygdala show strong expression of Neurogenin 2 and/or Semaphorin 5A, including the ventromedial claustrum and endopiriform nuclei, the lateral and basomedial amygdalar nuclei, the anterior and posteromedial cortical amygdalar areas, plus the amygdalo-hippocampal area. We interpret these nuclei or areas of the claustroamygdaloid complex as possible derivatives of the ventral pallium. In contrast, during embryonic development the dorsolateral claustrum, the basolateral amygdalar nucleus, and the posterolateral cortical amygdalar area do not express or show weak expression of Neurogenin 2 or Semaphorin 5A, but express selectively and strongly Cadherin 8 plus Emx1, and may be derivatives of the lateral pallium. The lateral pallial and ventral pallial divisions of the claustroamygdaloid complex appear to have some different sets of connections, although this requires further investigation.

Amygdala↗
PubMed2002

Expression profiling of lineage differentiation in pluripotential human embryonal carcinoma cells.

Pluripotential human embryonal carcinoma (EC) cell linesundergo differentiation programs resembling those occurring in embryonal stem cells during development. Expression profiling was performed during the terminal differentiation of the EC cell line, NTera2/Clone D1 by all-trans-retinoic acid. Time-response analysis via clustering of >12,000 human transcripts revealed distinct stages in the transition from an EC cell to neuronal progenitor cells expressing patterning markers compatible with posterior hindbrain fates followed by the appearance of immature postmitotic neurons with an evolving synaptic apparatus. Global analysis of gene expression allows monitoring cell fate and differentiation of EC cells in vitro and may provide insight into human embryonal stem cell development.

Antineoplastic Agents↗
PubMed2002

Stem-loop binding protein accumulates during oocyte maturation and is not cell-cycle-regulated in the early mouse embryo.

The stem-loop binding protein (SLBP) binds to the 3' end of histone mRNA and participates in 3'-processing of the newly synthesized transcripts, which protects them from degradation, and probably also promotes their translation. In proliferating cells, translation of SLBP mRNA begins at G1/S and the protein is degraded following DNA replication. These post-transcriptional mechanisms closely couple SLBP expression to S-phase of the cell cycle, and play a key role in restricting synthesis of replication-dependent histones to S-phase. In contrast to somatic cells, replication-dependent histone mRNAs accumulate and are translated independently of DNA replication in oocytes and early embryos. We report here that SLBP expression and activity also differ in mouse oocytes and early embryos compared with somatic cells. SLBP is present in oocytes that are arrested at prophase of G2/M, where it is concentrated in the nucleus. Upon entry into M-phase of meiotic maturation, SLBP begins to accumulate rapidly, reaching a very high level in mature oocytes arrested at metaphase II. Following fertilization, SLBP remains abundant in the nucleus and the cytoplasm throughout the first cell cycle, including both G1 and G2 phases. It declines during the second and third cell cycles, reaching a relatively low level by the late 4-cell stage. SLBP can bind the histone mRNA-stem-loop at all stages of the cell cycle in oocytes and early embryos, and it is the only stem-loop binding activity detectable in these cells. We also report that SLBP becomes phosphorylated rapidly following entry into M-phase of meiotic maturation through a mechanism that is sensitive to roscovitine, an inhibitor of cyclin-dependent kinases. SLBP is rapidly dephosphorylated following fertilization or parthenogenetic activation, and becomes newly phosphorylated at M-phase of mitosis. Phosphorylation does not affect its stem-loop binding activity. These results establish that, in contrast to Xenopus, mouse oocytes and embryos contain a single SLBP. Expression of SLBP is uncoupled from S-phase in oocytes and early embryos, which indicates that the mechanisms that impose cell-cycle-regulated expression of SLBP in somatic cells do not operate in oocytes or during the first embryonic cell cycle. This distinctive pattern of SLBP expression may be required for accumulation of histone proteins required for sperm chromatin remodelling and assembly of newly synthesized embryonic DNA into chromatin.

Animals↗
PubMed2005

A complex containing the Sm protein CAR-1 and the RNA helicase CGH-1 is required for embryonic cytokinesis in Caenorhabditis elegans.

Cytokinesis completes cell division and partitions the contents of one cell to the two daughter cells. Here we characterize CAR-1, a predicted RNA binding protein that is implicated in cytokinesis. CAR-1 localizes to germline-specific RNA-containing particles and copurifies with the essential RNA helicase, CGH-1, in an RNA-dependent fashion. The atypical Sm domain of CAR-1, which directly binds RNA, is dispensable for CAR-1 localization, but is critical for its function. Inhibition of CAR-1 by RNA-mediated depletion or mutation results in a specific defect in embryonic cytokinesis. This cytokinesis failure likely results from an anaphase spindle defect in which interzonal microtubule bundles that recruit Aurora B kinase and the kinesin, ZEN-4, fail to form between the separating chromosomes. Depletion of CGH-1 results in sterility, but partially depleted worms produce embryos that exhibit the CAR-1-depletion phenotype. Cumulatively, our results suggest that CAR-1 functions with CGH-1 to regulate a specific set of maternally loaded RNAs that is required for anaphase spindle structure and cytokinesis.

Anaphase↗
PubMedDate not supplied

Expression, action, and regulation of transforming growth factor alpha and epidermal growth factor receptor during embryonic and perinatal rat testis development.

The objective of the current study was to extend previous observations and examine the expression pattern and effects of transforming growth factor alpha (TGFalpha) and epidermal growth factor receptor (EGFR) on embryonic testis morphogenesis and growth. The expression of TGFalpha was determined after morphological sex determination (seminiferous cord formation at embryonic day 13 [ED13]) through perinatal testis development (postnatal day 5 [PD5]) with a quantitative reverse transcription-polymerase chain reaction procedure. Expression of messenger RNA (mRNA) for TGFalpha appeared to be more dynamic during testis development when compared with the expression of mRNA for EGFR. Message for TGFalpha was reduced at ED16 and PD4, and was elevated at PD0 during testis development. In contrast, EGFR mRNA levels were negligible at ED15 and were elevated constitutively from ED16 through PD5. Immunohistochemistry was conducted at ED14, ED16, ED19, PD0, PD3, and PD5 to localize cellular expression of both TGFalpha and EGFR. At ED16, positive staining for EGFR was localized to the cords, and by ED19, was mainly in the cords with slight expression in the interstitium. From PD0 to PD5, positive staining for EGFR was detected in the germ, Sertoli, and interstitial cells. Immunohistochemistry for TGFalpha detected localization at ED14 and ED16 to the Sertoli cells and to specific cells in the interstitium. From ED19 through PD5, TGFalpha was detected in the Sertoli, germ, and interstitial cells, and in endothelial cells within the interstitium. To determine the effects of TGFalpha on embryonic testis growth and seminiferous cord formation, ED13 testis organ cultures were treated with sense and antisense TGFalpha oligonucleotides. Antisense TGFalpha inhibited testis growth by 25%-30% in ED13 testis organ cultures when compared with sense oligonucleotide control pairs. To examine the effects of TGFalpha on perinatal testis growth, PD0 testis cultures were treated with different doses of TGFalpha. TGFalpha increased thymidine incorporation into DNA in PD0 testis cultures. Therefore, TGFalpha appears to have actions on both embryonic and perinatal testis growth. The regulation of TGFalpha and EGFR mRNA levels were examined using PD0 testis cultures treated with hormones that stimulate testis growth. Follicle-stimulating hormone (FSH) stimulated (P < .05) and testosterone tended to stimulate (P < .07) mRNA expression of EGFR. Epidermal growth factor stimulation of PD0 testis cultures did not affect levels of mRNA expression for EGFR, but did suppress expression of mRNA for TGFalpha. These results taken together demonstrate that TGFalpha can act to regulate early embryonic and perinatal testis growth. Furthermore, TGFalpha and EGFR expression can be regulated through growth stimulatory hormones such as FSH and testosterone.

Animals↗
PubMed2003

Establishment of POP-1 asymmetry in early C. elegans embryos.

In Caenhorabtidis elegans embryos, the nuclei of sister cells that are born from anterior/posterior divisions show an invariant high/low asymmetry, respectively, in their level of the transcription factor POP-1. Previous studies have shown that POP-1 asymmetry between the daughters of an embryonic cell called EMS results in part from a Wnt-like signal provided by a neighboring cell, called P(2). We identify here additional signaling cells that play a role in POP-1 asymmetry for other early embryonic cells. Some of these cells have signaling properties similar to P(2), whereas other cells use apparently distinct signaling pathways. Although cell signaling plays a critical role in POP-1 asymmetry during the first few cell divisions, later embryonic cells have an ability to generate POP-1 asymmetry that appears to be independent of prior Wnt signaling.

Animals↗
PubMed1979

The cellular effect of 5-bromodeoxyuridine on the mammalian embryo.

It is well known that 5-bromodeoxyuridine (BUdR) when injected into pregnant animals may cause exencephaly, cleft palate, and limb abnormalities. Similarly, it is well established that the drug when added to a culture medium may prevent differentiation of embryonic cell systems without affecting cell division or cell viability. The goal of our experiments was to examine whether the congenital malformations resulting from BUdR treatment were due to lack of differentiation of certain cell lines or were due to other mechanisms. The effects of BUdR on proliferating and differentiating cells in the 12-day mouse embryo were therefore examined and special attention was given to the proliferating cells of the rhombic lip which give rise to the Purkinje cells. When the embryos were treated with BUdR the mitotic index of the neuroepithelium of the rhombic lip doubled in value 3 h after treatment and remained high until 24 h later. By using the colchicine index it was calculated that the mitotic duration in the BUdR-treated embryos lasted at least 2 h and that in the control embryos less than 1 h. When the cell generation time in the BUdR treated animals was calculated the length of the S-phase was increased by about 50%. It was thus concluded that BUdR caused an increase in the duration of the S-phase and mitosis, together making the cell cycle 5 h longer than normal. Eighteen hours after treatment many neuroepithelial cells became degenerative. By radioautography it was demonstrated that the degenerating cells were in their second DNA-synthetic phase following BUdR injection and that cells which incorporated BUdR and were differentiating into neurons were not affected. By injecting [3H]BUdR it was found that many cells which incorporated the analogue were able to leave the proliferative population after their first cell division. They migrated to the periphery where they developed into apparently normal Purkinje cells. The additive effects of cell death and retardation of the cell cycle caused a 15% deficit of Purkinje cells in the postnatal cerebellum but the BUdR did not interfere with their differentiation. Thus, contrary to the BUdR effect on cultures of embryonic cells, in vivo the drug causes cell death and a delay in the cell cycle time. Our experiments therefore seem to indicate that the congenital malformations caused by BUdR in the mammalian embryo are caused by cell death and growth retardation rather than by interference with the process of differentiation.

Abnormalities, Drug-Induced↗
PubMed1985

The effect of surgical glove powder on cleavage of two-cell mouse embryos in an in vitro fertilization programme.

The effect of surgical glove powder on the development of early mouse embryos was studied. Embryos from F1 hybrid mice (C57 B1/6 X CBA) were suspended in Whittingham's T6 growth medium with 10% human serum, using Petri dishes (Falcon 3001). Contamination was brought about by a sterile, powdered, surgical glove touching the surface of the growth medium for less than a second in group I, and in group II the same procedure was followed but the glove was rinsed beforehand with sterile, four times distilled water and air-dried. In the control group (group III) no contamination with surgical glove powder occurred. In group I only 9 of 137 embryos (7%) reached the blastocyst stage, in contrast with 110 of 196 (56%) in group II and 258 of 287 (90%) in group III. The differences in results between groups I and III, groups I and II, and groups II and III were found to be statistically significant (P less than 0,001) by the chi-square test. It is concluded that surgical gloves are a potent inhibitor of early embryonic growth. In an in vitro fertilization programme including follicle aspiration and embryo transfer, contamination of embryos with these gloves should be avoided at all costs.

Animals↗
PubMed2003

Lineage allocation and asymmetries in the early mouse embryo.

The mouse blastocyst, at the time of implantation, has three distinct cell lineages: epiblast (EPI), trophoblast and primitive endoderm (PE). Interactions between these three lineages and their directional growth and migration are critical for establishing the initial asymmetries that result in anterior-posterior patterning of the embryo proper. We have re-investigated the timing of specification of the three lineages in relation to the differential allocation of progeny of the first two blastomeres to the embryonic versus abembryonic axis of the blastocyst. We find that the majority of cells of the inner cell mass (ICM) are specified to be EPI or PE by the mid 3.5 day blastocyst and that this is associated with localized expression of GATA-6 in the ICM. We propose a model for molecular specification of the blastocyst lineages in which a combination of cell division order, signal transduction differences between inner and outer cells and segregation of key transcription factors can produce a blastocyst in which all three lineages are normally set up in an ordered, lineage-dependent manner, but which can also reconstruct a blastocyst when division order or cell interactions are disturbed.

Animals↗
PubMed1997

Failure of neural tube closure in the loop-tail (Lp) mutant mouse: analysis of the embryonic mechanism.

Loop-tail (Lp) is unique among mouse mutants in failing to initiate neural tube closure at the cervical/hindbrain boundary (so-called 'Closure 1'), at the 5-7 somite stage. Lp/Lp embryos go on to develop a malformation that closely resembles cranio-rachischisis, the most severe neural tube defect found in humans. We investigated several possible embryological mechanisms that may underlie this failure of neural tube closure in Lp. The genotypes of Lp/Lp, Lp/+ and +/+ embryos from mixed litters were identified using the polymerase chain reaction to amplify a polymorphic microsatellite sequence that is very closely linked to Lp. At post-neurulation stages of development, Lp/Lp embryos have a shortened body axis, which could suggest a defect of axial elongation as the primary anomaly in Lp. However, we found that axial elongation is normal in Lp homozygotes prior to the stage of defective Closure 1, indicating that the shortened body axis of later embryos is a secondary effect of the neurulation anomaly, or an independent effect of the Lp mutation. Some workers have reported cell proliferation rates to be abnormal in later stage Lp/Lp embryos. We observed variations in [3H]thymidine labelling index, and mitotic index, between embryonic tissues, and between embryos at different somite stages. However, Lp/Lp, Lp/+ and +/+ embryos had closely similar cell proliferation parameters, arguing against a mechanism based on faulty embryonic growth. Thirdly, we tested the hypothesis that the defect in loop-tail results from an inability of the neural folds to become apposed, specifically at the site of Closure 1. By tying a silk suture around the embryonic axis, at the future site of Closure 1, we were able to effect convergence of the neural folds at this site. Neural fold closure failed to progress along the body axis in sutured Lp/Lp embryos, however, in contrast to operated Lp/+ and +/+ embryos which exhibited normal progression of neural tube closure. The embryonic defect in loop-tail appears, therefore, to involve either a general inability of the spinal neural folds to become apposed along the spinal region, or a defect in the process of neural fold fusion.

Animals↗
PubMed1994

Developmentally timed expression of an embryonic growth phenotype in vascular smooth muscle cells.

Little is known about the phenotypic changes that occur in vascular smooth muscle cells (SMCs) as the developing aorta undergoes the transition from a loosely organized, highly replicative tissue to a morphologically mature, quiescent tissue. In the present study, we have characterized the in vivo pattern of SMC replication during intrauterine and neonatal aortic development in the rat and have cultured and assessed the in vitro growth properties of embryonic, fetal, and neonatal vascular SMCs. Embryonic SMCs, which exhibited a very high in vivo replication rate (75% to 80% per day), demonstrated a significant potential for self-driven replication, as assessed by the ability to proliferate under serum-deprived conditions. Several lines of evidence suggest that the autonomous growth of SMCs in the "embryonic growth phenotype" may be driven by a unique mechanism independent of known adult SMC mitogens: embryonic SMC replication was not associated with the detectable secretion of mitogenic activity capable of stimulating adult SMCs, and embryonic SMCs were mitogenically unresponsive to a variety of known adult SMC growth factors. The capacity for self-driven growth was lost by embryonic day 20, suggesting that important changes in gene expression and phenotype occur in developing SMCs between embryonic days 18 and 20. Taken together, the data describe a unique embryonic growth phenotype of vascular SMCs and suggest that the replication of aortic SMCs during intrauterine development is self driven, self regulated, and controlled by a developmental timing mechanism. The conversion of SMCs from the embryonic to the late fetal/adult growth phenotype will likely be found to be an important component of a developmental system controlling vascular morphogenesis.

Animals↗