No description available.

No description available.

No description available.

Class of 2009 Abstract / OBJECTIVES: The objective of this study was to characterize the Hyaluronidase (HYA) gene family throughout gestational development of murine hearts to provide greater insight regarding its role in cardiac morphogenesis. METHODS: Microdissection of murine embryos was accomplished to extract embryonic heart tissue. RNA was extracted using the standard Trizol protocol. cDNA templates were created using a standard protocol. Polymerase chain reaction (PCR) was used to verify presence of HYA, isolate a sample for insertion into a cloning plasmid to make a recombinant clone. A TOPO cloning reaction followed by a double DNA digest was accomplished to verify gene sequencing and orientation in the clone. SYBR Green real time RT- PCR was used to quantify gene expression relative to 18S RNA. RESULTS: RT-PCR provided qualitative data indicating HYA1, HYA2, and HYA3 are present at all observed time points (E8.5, E9.5, E10.5, E11.5, E12.5, E13.5, E14.5, E15.5, and E16.5). Real time RT-PCR data results characterizing relative expression for HYA2: E9.0 (Rel. Exp. = 1.00; SD = 0), E10.5 (Rel. Exp. = 1.33; SD = 0.577), E12.5 (Rel. Exp. = 2.00; SD = 0), E13.5 (Rel. Exp. = 2.66; SD = 0.577), E14.5 (Rel. Exp. = 3.00; SD = 0), E15.0 (Rel. Exp. = 2.00; SD = Error). CONCLUSIONS: HYA1, HYA2, and HYA3 are present at al time points observed in embryonic heart tissue. Relative expression of HYA2 progressively increased from E9.0 until E14.5 and then started tapering downward at time point E15.0.

The onset of agriculture about 12,000 years ago has had a major influence on the biodiversity of plants and animals. Unfortunately, the rapid changes in agricultural practices that has occurred in recent times has negatively affected many farmland species. One such species is the grass snake (Natrix natrix), which has been reported to decline in many parts of Europe, including Sweden. The grass snake is unique, not only in that it is the most northerly distributed oviparous reptile in the world, but also because of its habit of using anthropogenic heat sources such as manure heaps and composts as nesting-sites. Unfortunately changes in manure management and abandonment of farmlands have resulted in a decline and fragmentation of these environments. This may pose a threat for the northernmost populations of the grass snake, because natural nests in these areas may not provide sufficient heat for the eggs to hatch. The eggs and embryos of reptiles are highly sensitive to incubation temperatures, which can influence not only hatching success but also many phenotypic traits in the hatchlings. In this thesis I used a series of laboratory and field experiments to investigate the importance of anthropogenic heat sources for the reproductive ecology of cold-climate populations of grass snakes.  More specifically, I aimed to investigate thermal regimes of nests and how they influence embryonic development and offspring traits associated with survival and fitness. The results showed that manure heaps and composts are significantly warmer than potential natural nests and that natural nests do not provide sufficient heat to sustain embryonic development. Further, manure heaps were warmer and more constant in temperature than composts, resulting in higher hatching success and earlier hatching in manure heaps. The higher thermal variability in composts increased the frequency of abnormalities that are likely to negatively affect survival and fitness. In conclusion, this thesis shows that the use of anthropogenic heat sources has enabled grass snakes to expand their range farther north than any other oviparous reptile and that the thermal dichotomy in the primary nesting environments used by grass snakes contribute to important life-history variation in this species. These findings have important implications for conservation of reptile populations in general and grass snakes in particular.

Thesis (Ph. D.)--Cornell University, January, 2009. / Vita. Includes bibliographical references (leaves 180-186).

Thesis (M.Sc.) Uppsala : Sveriges lantbruksuniv.

Diss. (sammanfattning) Göteborg : Göteborgs universitet, 2008. / Härtill 3 uppsatser.

The aim of his study was to investigate the role of Dctn2 in mouse preimplantation embryonic development, specifically its effect on the first cell fate decision, when the number of cells increases from eight to sixteen.

Fetal growth restriction (FGR) is the failure of a fetus to reach its pre-determined genetic growth potential during development. FGR is associated both with poor outcome in the neonatal period, and the onset of major adult diseases such as diabetes, hypertension and obesity. Therefore understanding what causes restricted fetal growth is important both for improving neonatal health, and for the minimization of major worldwide healthcare burdens. Described here are two mutant mouse lines, each with a distinct mutation in the Mediator complex gene Med31. These mutations result in reduced fetal growth, allowing for the investigation of the role of Med31 in the proper control of growth during development. The first mutant mouse line (Med31 Null) carries a C/T point mutation in exon 4 of Med31. Homozygous mutant embryos display reduced growth during development, characterized by their reduced size and smaller forelimbs compared to their heterozygous littermate controls. The second mutant mouse line (Med31 Y57C) carries a T/C point mutation in exon 3 of Med31. Similarly, homozygous mutant embryos display reduced fetal growth with reductions in forelimb length compared to their heterozygous littermate controls. In both mutant lines whole embryo growth and endochondral ossification within the limbs is perturbed. This is due to defects in cellular proliferation and the misexpression of the cell cycle genes Ccnb1 and Mtor within the mutant embryos. Additionally, the Med31 Null line is embryonic lethal by E18.5 and displays morphological defects of the placenta compared to heterozygous littermate controls. These morphological differences are suggestive of defects in the function of the placenta, and are proposed as the cause of embryonic lethality. In support of this the Med31 Y57C line is viable with no defects in placental development. New roles for Med31 in embryonic growth, cellular proliferation and placental development are identified. Moreover the two mutant lines constitue an allelic series of Med31, and the two mutations provide insights into the various ways Med31 is able to regulate transcription during development.