Tag: Poster 88

Land-Seizing Language: Rhetoric’s Claim to Territory in Colonial Travel Writing of the New World

Presenter: Erin Weaver

Faculty Mentor: Elizabeth Bohls, Brent Dawson

Presentation Type: Poster 88

Primary Research Area: Humanities

Major: English

England sends its first party of settlers to New World Virginia in 1585, but it isn’t until 1607 that the empire founds Jamestown – the first lasting colony on the continent, following 22 years of failure to occupy the territory. In absence of physical ownership of the land, how to do the narratives that emerge out of the New World during this period attempt to assert a rhetorical claim to it?

To answer this question, my research analyzes the writing of New World authors Smith, White, Lane, and Harriot. Thus far, it has investigated the existence of the following through close reading analysis in order to pinpoint rhetorical strategies that assert possession: a) the binding of space in the New World into definable (and therefore claimable) place through rhetorical cartography and the theory of space and place; b) Edenic tropes to assert a God-given right to cultivate the landscape and mark it as claimed; c) syntactical structures that infantilize native improvements and project English structures (or signs of ownership) onto the land.

The rhetoric of travel writing has been well studied; the rhetoric of claim within these texts is lacking. In combining the studies of travel writing’s rhetoric and language’s ability to bound space, I will discern ways in which English colonists are able to claim the territory solely through their use of narrative.

Severity of Cranial Phenotypes in Double Mutants Affected by the Interaction Between fras1 and ezh2 Genes

Presenter(s): Samuel Ahlquist – Human Physiology

Co presenter(s): Whitney Olivia

Faculty Mentor(s): Charles Kimmel

Poster 88

Research Area: Biology

This study assesses the interaction between two genes, fras1 and ezh2, in zebrafish craniofacial patterning. The Fras1 protein stabilizes facial development and is studied to understand Fraser syndrome in humans. Ezh2 is a protein subunit of a repressive complex that is important for early embryonic development and essential for tissue maintenance. Ezh2 is explored because of its role in controlling epigenetics, which is a background that can affect the expression of genes. Loss of function in these two genes individually results in mild reduction in the opercular bone (OP). We therefore hypothesized that the interaction between ezh2 and fras1 in double mutants will result in more severe reduction in OP bone size. Zebrafish embryos were stained to assess bone morphology and each set was phenotypically separated into WT, single, and double mutant groups using key phenotypes. The embryos will be genotypically verified through PCR in this ongoing study. As predicted, the double mutants displayed more severe reduction in the OP bone when compared to the single mutants. We concluded that the double mutants displayed a synergistic effect for the OP bone as the result appears more severe than both single mutants combined. This study suggests that changes in epigenetics, in this case loss of ezh2 function, influences the severity of the fras1 phenotype which could also influence the degree of severity of Fraser syndrome in humans.