Thesis (M.S.)--Missouri State University, 2008. / "August 2008" Includes bibliographical references (leaves 31-36). Also available online.

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The detrimental effects of oxidative stress caused by the accumulation of Reactive Oxygen Species (ROS) have been acknowledged as major factors in aging, senescence and several neurodegenerative diseases and conditions such as Parkinson’s disease and stroke (ischemia/reperfusion). Mammalian models are extremely susceptible to these stresses that follow the restoration of oxygen after anoxia; however, some organisms including the freshwater turtle Trachemys scripta can withstand several bouts of anoxia and repeated reoxygenation without any apparent pathology. T. scripta thus provides us with an alternate vertebrate model in which we can investigate physiological mechanisms of neuroprotection without the damaging effects that come with oxidative stress. The major objective of this study was to investigate the protective mechanisms in the turtle brain under conditions of anoxia and oxidative stress. Specifically, the focus is on the Methionine Sulfoxide Reductase system (Msr), an antioxidant and cellular repair system, and how it is regulated to protect the brain against such stressors. Previous studies in my lab have demonstrated that Msr mRNA and protein levels are differentially upregulated during anoxia and reoxygenation. To investigate the regulation of Msr, FOXO3a was directly induced by transfecting a human FOXO3a plasmid into turtle brain cell cultures, as FOXO3a has been shown to regulate MsrA levels in other animal models. Pharmacological manipulation of FOXO3a was also performed using the green tea extract Epigallocatechin gallate (EGCG) as it has been shown to increase expression of FOXO3a during oxidative stress conditions in other models. I found that an induction of human FOXO3a increased FOXO3a levels and showed protection against cell death during oxidative stress. Furthermore, treatment of cells with EGCG increased expression of FOXO3a only when the cells were exposed to oxidative stress and decreased cell death. Induction of FOXO3a and EGCG treatment did not increase MsrA levels, however MsrB3 levels were upregulated under both treatments but only in the presence of oxidative stress. These results suggest that MsrA and MsrB3 protect the cells from oxidative stress damage through different molecular pathways and that EGCG may be a therapeutic target to treat diseases related to damage by oxidative stress. / Includes bibliography. / Dissertation (Ph.D.)--Florida Atlantic University, 2018. / FAU Electronic Theses and Dissertations Collection

<p>A unique feature of the fetal gonad is its ability to form two distinct organs, the testis and the ovary, from a single bipotential primordium. The outcome of this decision, which is made by a population of somatic cells known as the bipotential supporting cell precursors, determines whether an embryo will develop as a phenotypic male or female. Though several molecular pathways have been shown to be required for female fate determination in vertebrates, the intricacies of ovarian morphogenesis are not well understood. A key event in ovarian development occurs around birth, when meiotic germ cells and somatic granulosa cells organize into primordial follicles, the structures that generate mature oocytes for ovulation in adult females. We investigated the embryonic origins and proliferative properties of granulosa cells in the fetal mouse ovary and found that the precursors emerge from the ovarian surface epithelium and then enter mitotic arrest in a specification process that extends from the bipotential stage to the end of the postnatal follicle assembly period. Maintenance of cell cycle arrest in granulosa cell precursors appears to be regulated by Wnt signaling. The first granulosa cells to be specified were exclusively incorporated into the subset of follicles that begin to grow immediately upon assembly. We show that this first group of granulosa progenitors derives from the supporting cell precursors present in the bipotential gonad. Interestingly, both XX and XY supporting cell precursors were mitotically arrested towards the end of the bipotential period, indicating that adoption of supporting cell fate might be regulated by the cell cycle. We also show that antagonism of Notch signaling may be required for these precursor cells to exit the cell cycle and differentiate.</p><p>In Witschi's classic model of vertebrate gonad development, the cortex and medulla of the undifferentiated gonad expand and differentiate in a mutually exclusive manner to yield the mature ovary and testis (Witschi 1951). Estrogen acts on both the cortex and medulla to promote female fate determination and ovary development in non-mammalian vertebrates. However, the downstream receptors and targets through which estrogen exerts its effects on the gonad have not yet been elucidated. We selected the red-eared slider turtle Trachemys scripta as a model with which to address this question. We first characterized the cellular composition of the turtle gonad before and after sex determination, identifying four populations of somatic cells distinguishable by their location within the gonad as well as the complement of transcription factors expressed. This information was then applied to an investigation of estrogen signaling pathways in the turtle ovary. We show that i) estrogen likely acts through its canonical receptors rather than a non-canonical pathway involving ERK signaling; ii) early exposure to estrogen resulted in the premature downregulation of a testis-specific gene, SOX9, in the medulla; iii) less estrogen is needed to promote ovarian differentiation in the cortex of the gonad than to repress testicular differentiation of the medulla, consistent with the localized production of estrogen in the medulla; and iv) estrogen's repressive effect on SOX9 expression may be mediated by Wnt signaling. </p><p>Our findings add complexity to the standard model of how the male and female supporting cell lineages are established in mice, reveal evolutionary conservation between mice and turtles in the timing of granulosa cell specification relative to sex determination., and refine our understanding of how estrogen acts to promote ovarian development in non-mammalian species.</p> / Dissertation

Thesis (M.S.)--Ohio University, June, 2006. / Title from PDF t.p. Includes bibliographical references (p. 104-111)

Thesis (M.S.)--Texas State University-San Marcos, 2008. / Vita. Includes bibliographical references (leaves 22-25). Also available on microfilm.

Thesis (Ph.D.)--Ohio University, August, 2006. / Title from PDF t.p. Includes bibliographical references.

<p>Sex determination is a critical biological process for all sexually reproducing animals. Despite its significance, evolution has provided a vast array of mechanisms by which sexual phenotype is determined and elaborated even within amniote vertebrates. The most prevalent systems of sex determination in this clade are genetic and temperature dependent sex determination. These two systems are sometimes consistent within large groups of species, such as the mammals who nearly ubiquitously utilize XY genetic sex determination, or they can be much more mixed as in reptiles that use genetic or temperature dependent systems and even both simultaneously. The turtles are a particularly diverse group in the way they determine sex with multiple different genetic and temperature based systems having been described. We investigated the nature of the temperature based sex determination system in Trachemys scripta elegans to ascertain whether it behaved as a purely temperature based system or if some other global source of sex determining information might be apparent within thermal regions insufficient to fully induce male or female development. These experiments found that sex determination in this species is much more complex and early acting than previously thought and that each gonad within an individual has the same sexual fate established enough that it can persist even without further communication between. We established a best practice for the assembly and annotation of de novo whole transcriptomes from T. scripta RNA-seq and utilized the technique to quantify the gene regulatory events that occur across the thermal sensitive period.</p><p>Evidence is entirely lacking on the resolution of TSD when eggs are incubated at the pivitol temperature in which equal numbers or males and females are produces. We have produced a timecourse data set that allowed for the elucidation of the gene expression events that occur at both the MPT and FPT over the course of the thermal sensitive period. Our data suggests that early establishment of a male or female fate is possible when temperature is sufficiently strong enough as at MPT and FPT. We see a strong pattern of mutually antagonistic gene expression patterns emerging early and expanding over time through the end of the period of gonad plasticity. In addition, we have identified a strong pattern of differential expression in the early embryo at stages prior to the formation of the gonad. Even without the known systemic signaling attributed to sex hormones emanating from the gonad, the early embryo has a clear male and female gene expression pattern. We discuss how this early potential masculinization or feminization of the embryo may indicate that the influence of temperature may extend beyond the determination of gonadal sex or even metabolic adjustments and how this challenges the well-defined paradigm in which gonadal sex determines peripheral sexual characteristics.</p> / Dissertation

Programa de Doctorado: Biotecnología en ciencias de la salud (Biotecnología y Bíomedicina)