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PubMed2004

Increased expression of insulin-like growth factor-I (IGF-I) during embryonic development produces neocortical overgrowth with differentially greater effects on specific cytoarchitectonic areas and cortical layers.

The in vivo actions of insulin-like growth factor-I (IGF-I) on the growth and development of the cerebral cortex were investigated in transgenic (Tg) mice that overexpress IGF-I in the brain, beginning as early as embryonic day (E) 13. Compared to non-Tg littermate controls, Tg mice at postnatal day (P) 12 exhibited significant increases in total cortical volume (31%) and in total neuron number (27%). The numerical density of neurons did not differ significantly between Tg and control mice, except in layer I. Comparing cytoarchitectonic areas in Tg mice, significantly greater increases in cortical volume were found for the motor cortex (42%), compared to somatosensory cortex (35%). Similarly, greater increases in total neuron number were found for motor cortex (44%) compared to somatosensory cortex (28%). Comparing individual cortical layers in Tg mice, the greatest increase in neuron number was found in layer I for both motor (93%) and somatosensory (76%) regions, followed by layer V (36-53%)>II/III (26-47%)>VI (26-37%)>IV (22-34%). Our results demonstrate that increased expression of IGF-I in vivo during embryonic and early postnatal development produces substantial overgrowth of the neocortex. IGF-I-mediated growth and development exhibits differential effects in some cytoarchitectonic areas and in lamina-specific neuron populations, most notably the neurons of layer I.

Age Factors↗
PubMed1989

Embryonic development of the chick primary trigeminal sensory-motor complex.

The objective of this study is to define the development of all components in the chick embryonic trigeminal primary sensory-motor complex, from their first appearance through the formation of central and peripheral axonal projections up to stage 34 (8 days of incubation). This was accomplished by two labeling procedures: application of the monoclonal antibody HNK-1, which binds to the precursors of all these components except the placode-derived neurons, and application of HRP to axons cut immediately distal to the trigeminal ganglion. Single immunopositive motor neuron precursors are present at stage 12. These accumulate in the transient medial motor column, whose neurons initiate axon outgrowth by stage 13-14, concomitant with the onset of translocation of their somata to form the definitive trigeminal lateral motor column (LMC). Initially these translocating somata accumulate on the medial margin of the LMC. Beginning on incubation day 5, axons growing from newly formed motor neurons pass beside the lateral margin of the LMC, and the nuclei of these cells subsequently follow this pathway. These events follow a rostral-to-caudal sequence, and this phase of motor nucleus formation is complete by day 8. The lateral translocation of some caudally located nuclei is arrested beginning on day 5. This cessation, which proceeds rostrally, demarcates neurons that form the dorsal motor nucleus of the trigeminal complex. Sensory neurite formation is initiated in ophthalmic placode-derived cells at stage 14.5, one stage later by maxillomandibular neurons, and from mesencephalic V cells at stage 15. Neural crest cells do not initiate axon formation until at least day 4 to 5. Following application of HRP distal to the condensing ganglion at stage 16, labeled ophthalmic nerve projections appear in contact with the wall of the hindbrain centrally and overlying the optic vesicle peripherally. Fibers forming the descending tract elongate rapidly, reaching the level of the VIIth nerve root (200 microns caudal to the trigeminal root) by stage 18 and the cervical cord by stage 22. Labeled terminal arborizations of descending trigeminal afferents are first visible at stage 22 and are evident along the entire descending and proximal ascending tracts by stage 27. Later-developing descending axons grow in close association with existing trigeminal fibers, though a few growth cones are consistently evident superficial to the other fibers. No projections different from those reported in adult birds are seen, nor are there any contralateral afferent projections.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed2004

SRF regulates Bcl-2 expression and promotes cell survival during murine embryonic development.

The transcription factor serum response factor (SRF) controls the expression of genes involved in cellular proliferation and differentiation. Interestingly, SRF also promotes cell survival by regulating the expression of antiapoptotic genes. In in vitro differentiating murine embryonic stem (ES) cells, SRF deficiency leads to increased apoptosis. Loss of SRF correlates with impaired expression of the antiapoptotic Bcl-2 and Bcl-xl genes. SRF binds the Bcl-2 promoter in vivo and activates Bcl-2 transcription. Reconstituting Bcl-2 in Srf-/- ES cells rescues these cells from apoptosis, demonstrating that SRF-dependent Bcl-2 expression is critical for ES cell survival. At the multicellular level, SRF deficiency leads to impaired cavitation and reduced Bcl-2 expression in embryoid bodies (EBs) and inappropriate apoptosis in both EBs and pregastrulation mouse embryos. Thus, our data from genetic and cellular studies uncover SRF-regulated Bcl-2 expression as a novel mechanism that is important for cell survival during early murine embryogenesis.

Animals↗
PubMed2005

[Effects of ginsenoside Rb1 on mouse embryonic development in vitro].

OBJECTIVE: To evaluate the developmental toxicity of ginsenoside Rb1 and the potential mechanism of it in vitro. METHODS: Whole embryo culture system was used in this research. Embryos were exposed to various concentrations of ginsenoside Rb1, and scored for growth and development at the end of the 48h culture period. RESULTS: With the concentration of Rb1 rising, the total morphological scores significantly decreased; Developments of forebrain, midbrain and optic system were relatively sensitive to Rb1 and were affected at the concentration of 30 microg/ml; hindbrain, Branchial arch and limb buds were affected at 50 microg/ml; Yolk sac was affected at the low concentration of 15 microg/ml and the indexes of embryonic growth and development decreased at the high concentration of 50 microg/ml. Moreover, the rate of embryo teratogenicity were obviously increased. CONCLUSION: Ginsenoside Rb1 displayed teratogenic action in mice. The damage on structure and function of yolk sac might be part of teratogenic mechanisms of it.

Abnormalities, Drug-Induced↗
PubMed2006

Three Dact gene family members are expressed during embryonic development and in the adult brains of mice.

Members of the Dact protein family initially were identified through binding to Dishevelled (Dvl), a cytoplasmic protein central to Wnt signaling. During mouse development, Dact1 is detected in the presomitic mesoderm and somites during segmentation, in the limb bud mesenchyme and other mesoderm-derived tissues, and in the central nervous system (CNS). Dact2 expression is most prominent during organogenesis of the thymus, kidneys, and salivary glands, with much lower levels in the somites and in the developing CNS. Dact3, not previously described in any organism, is expressed in the ventral region of maturing somites, limb bud and branchial arch mesenchyme, and in the embryonic CNS; of the three paralogs, it is the most highly expressed in the adult cerebral cortex. These data are consistent with studies in other vertebrates showing that Dact paralogs have distinct signaling and developmental roles and suggest they may differentially contribute to postnatal brain physiology.

Adaptor Proteins, Signal Transducing↗
PubMed2002

[Effects of simulated microgravity on preimplantation embryonic development of Kunming mouse in vitro].

In order to investigate the development of Kunming mouse preimplantation embryos cultured in vitro under simulated microgravtiy, one-cell and 4-cell embryos of Kunming mouse (Fertilization In Situ) were cultured in CZB or KSOM media under simulated microgravity or normal gravity environment respectively. The results showed that under normal gravity, the percentage of passing 2-cell development block embryos was not different in CZB with in KSOM, but the percentage of blastocysts was lower in CZB than that in KSOM significantly. The percentages of passing 2-cell development block embryos and blastocysts in CZB or KSOM were lower under simulated microgravity than those under normal gravity. It is suggested that the frequency of early embryonic lethality is possibly increased by simulated microgravity.

Animals↗
PubMed2001

Ubiquinone is necessary for mouse embryonic development but is not essential for mitochondrial respiration.

Ubiquinone (UQ) is a lipid found in most biological membranes and is a co-factor in many redox processes including the mitochondrial respiratory chain. UQ has been implicated in protection from oxidative stress and in the aging process. Consequently, it is used as a dietary supplement and to treat mitochondrial diseases. Mutants of the clk-1 gene of the nematode Caenorhabditis elegans are fertile and have an increased life span, although they do not produce UQ but instead accumulate a biosynthetic intermediate, demethoxyubiquinone (DMQ). DMQ appears capable to partially replace UQ for respiration in vivo and in vitro. We have produced a vertebrate model of cells and tissues devoid of UQ by generating a knockout mutation of the murine orthologue of clk-1 (mclk1). We find that mclk1-/- embryonic stem cells and embryos accumulate DMQ instead of UQ. As in the nematode mutant, the activity of the mitochondrial respiratory chain of -/- embryonic stem cells is only mildly affected (65% of wild-type oxygen consumption). However, mclk1-/- embryos arrest development at midgestation, although earlier developmental stages appear normal. These findings indicate that UQ is necessary for vertebrate embryonic development but suggest that mitochondrial respiration is not the function for which UQ is essential when DMQ is present.

Animals↗