No description available.

All the tissues within the developing embryo are comprised of cells formed from one of the three germ layers defined during gastrulation; the ectoderm, mesoderm and endoderm. Understanding how the germ layers are formed and subsequently differentiate into different tissues is the basis of developmental biology.

Embryonic exposure to the anticonvulsant drug Dilantin has been shown to have detrimental effects on development. Some of the observed effects include growth retardation, craniofacial defects, and even death. As the drug is metabolized, toxic intermediates form, which could be causing the characteristic abnormalities observed in embryos exposed to Dilantin. Culture of preimplantation mouse embryos in the presence of IOµg/mL or 20µglmL Dilantin show a slowing of development inl9.3% and 19.1% ofembryos respectively at Day 3 of culture. The toxic intermediates could be causing alterations in cyclin expression, cell cycle proteins, or the cell cycle timing itself. Previous research determined an in vivo baseline expression for cyclins B 1, E, D, A and cdk2, which was used to compare the expression of these cyclins and cdks between in vivo and Dilantin cultured embryos. Altered patterns in cultured embryos suggested that an alteration in cell cycle timing, therefore, S phase timing was determined in cultured untreated embryos utilizing 5'-Bromo-2-deoxyuridine (BrdU) incorporation and indirect immunofluorescence staining. The results of the experiment showed the second S phase was at 30 hpf, approximately 9 hours later, and the third S phase was at 54 hpf, approximately 3 hours later than previous in vivo literature reports. S phase timing in NaOH vehicle controls did not appear different from untreated controls. Dilantin showed S phase peaks at 24 and 55 hpf. In the Dilantin treated embryos, the nuclear staining intensity for the second S phase did not decrease as rapidly as had been observed in control embryos. Embryos that developed beyond the 2-cell stage demonstrated two distinct S phase peaks at 45 and 54 hpf, while embryos at the 2-cell stage did pass through the second S phase but not the third S phase. These data suggested that the Dilantin could be causing a delay in G2. Future experiments would be necessary to determine if the expression of G2 cyclins are being altered in Dilantin treated embryos. / Department of Biology

The Drosophila embryo is patterned by a complex interplay of zygotically expressed genes and maternally supplied components, a large number of which have been identified. However, many maternal components are encoded by essential zygotic genes whose maternal effects are not amenable to conventional genetic analysis. Investigation of such genes requires the generation of homozygous mutant germ cells in chimeric females, and analysis of their embryos. The recent development of techniques which allow the efficient generation of germline clones has made the screening of zygotic lethal mutations for maternal effects more feasible. I have generated a collection of X-linked zygotic lethal mutations and used FLP recombinase catalysed mitotic recombination to look for maternal effects affecting segmentation. Two mutations have been recovered which have maternal effect phenotypes similar to those of the pair-rule segmentation genes. The leprechaun mutation affects oogenesis, so fertile females are very rare, preventing straightforward phenotypic analysis of the segmentation phenotype. Attempts to generate a rescuing duplication are described. The second mutation, stunted (sun), initially gave rise to a segmentation cuticle phenotype. Subsequent attempts to reproduce the phenotype were unsuccessful as it was masked by a severe reduction in the amount of cuticle secreted, a phenotype characteristic of the neurogenic genes. Detailed analysis revealed that the primary lesion affects neither segmentation or neurogenesis. Rather, sun⁺ is required for cellularisation of the syncytial blastoderm and for the localisation of actin to 'caps' above the syncytial nuclei. Cloning of a candidate gene for stunted revealed a predicted protein product limited homology to cyclins. In addition to searching for novel segmentation genes, potential proteinprotein interactions of the segmentation gene hairy's protein product were also investigated, and a model is presented for its mode of action as a transcriptional repressor.

No description available.

No description available.

The importance of hormone reservoirs in mature teleost eggs is unknown. To elucidate the effects of hormones on embryonic development, steelhead trout eggs, Oncorhynchus mykiss, were immersed in either cortisol, testosterone, or thyroxine at two different stages of development. Elevated concentrations of cortisol were detectable in the trout eggs or embryos after immersion. Eggs exposed to cortisol during water hardening hatched faster than eggs exposed at the eyed stage. Eggs that hatched faster had elevated cortisol and cortisol glucuronide concentrations at hatch compared to groups immersed at eyed or control groups. The dedine of these elevated concentrations of cortisol and cortisol glucuronide during embryonic development suggest conversion, clearance or both. Eggs exposed to cortisol at the earlier developmental stage did not appear to clear or convert cortisol as efficiently as those exposed at a later stage. Testosterone did not accelerate hatching in steelhead trout. Thyroxine accelerated hatching in eggs immersed at the eyed stages but had no effect when given at water hardening. These eggs that hatched faster were more synchronous in hatching time compared to other groups. Prior to exogenous feeding (50 days post fertilization, dpf), animals immersed in cortisol when eye pigments had higher mean condition factor (Kn) than other experimental or control groups, but this effect was gone by 83 dpf. However, at 130 dpf, cortisol groups that were immersed at the eyed stage were again heavier, longer, and more robust than other groups. At 50 dpf, animals immersed in thyroxine at water hardening were significantly longer and less robust (smaller condition factor, Kn). These effects disappeared by 83 dpf. / Graduation date: 1993

Thesis (Ph. D.)--University of Chicago. / Reprinted from the Botanical Gazette, Vol. XLVI, No. 3, pp. 161-178. "Literature cited" p. 176. Also available on the Internet.

Diss. (sammanfattning) Stockholm : Karol. inst. / Härtill 4 uppsatser.

Thesis (Ph. D.)--University of Chicago. / "Reprinted from the Botanical gazette, September and October, 1899." Includes bibliographical references (p. 41-42). Also available on the Internet.