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Anthropology - Butler University

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European species Chara canescens were used to attempt DNA amplification in Chara brittonii<br />

and several other closely related species. Lack of amplification suggests that North American<br />

and European species are too distantly related for primer recognition. A Hanes Trust Grant has<br />

recently provided funding to develop species-specific primers for Chara brittonii and the related<br />

species Chara zeylanica at the Savannah River Ecology Lab (<strong>University</strong> of Georgia) using stateof-the-art<br />

Illumina paired-end sequencing. This will result in the production of 36 primers per<br />

species which will then be screened and optimized to identify those with the greatest<br />

polymorphism.<br />

mTOR Signaling Mediates TBI-enhanced Neural Stem Cell Proliferation<br />

Pich Seekaew, Faculty Sponsor: Jinhui Chen, Indiana <strong>University</strong>/Purdue <strong>University</strong> at<br />

Indianapolis<br />

Traumatic Brain Injury (TBI) induced neuron death was once thought to be irreversible.<br />

However, the identification of neural stem cells (NSCs) in the adult brain holds the hope of<br />

repairing injured brain following TBI. Our previous study showed that TBI promotes NSC<br />

proliferation in an attempt to initial an innate repair and/or plasticity mechanisms. However, this<br />

induced proliferation is transient without significantly increasing neurogenesis. It suggests that<br />

additional intervention is required to further increase NSC proliferation to enhance neurogenesis<br />

for successfully repairing the damaged brain following TBI. In order to determine the molecular<br />

mechanism that mediates TBI-enhanced NSC proliferation, we assessed the activity of<br />

mammalian target of rapamycin (mTOR) signaling by detecting the level of Phospho-S6<br />

Ribosomal protein (pS6), an indicator of the activity of mTOR signaling. We found that the level<br />

of pS6 was transient but dramatically increased prior to TBI-enhanced NSC proliferation. In<br />

contrast inhibiting the activity of mTOR signaling with rapamycin attenuated this effect,<br />

indicating that mTOR signaling mediates TBI-enhanced NSC proliferation. Further stimulating<br />

mTOR signaling strengthened the effect of TBI-enhanced NSC proliferation. These results<br />

suggest that mTOR signaling mediates TBI-enhanced neural stem cell proliferation and<br />

stimulating mTOR signaling may be a potential therapeutic approach to enhance neurogenesis<br />

for post-traumatic functional recovery.<br />

Identification of Transcription Factors Associated with Down Syndrome Skeletal<br />

Abnormalities<br />

Nicole Shepherd, Faculty Sponsor: Randall Roper, Indiana <strong>University</strong>/Purdue <strong>University</strong> at<br />

Indianapolis<br />

Individuals with Down syndrome (DS) exhibit a variety of phenotypes, including craniofacial<br />

and skeletal dysmorphologies. It is believed that trisomic genes initiate phenotypes associated<br />

with Down syndrome, though specific gene-phenotype relationships for DS are largely<br />

unknown. We hypothesize that the altered expression of genes in three copies will also affect the<br />

expression of downstream genes, including non-trisomic genes and play an important role in DS<br />

phenotypes. Transcription factors, which encode proteins that bind to specific DNA sequences<br />

controlling the flow of transcription, are among the genes that may be affected by trisomy. We<br />

have identified genetic and phenotypic alterations in craniofacial precursors as early as<br />

embryonic dayE9.5of the Ts65Dn mouse model of human DS. This mouse model is trisomic for<br />

orthologs of approximately half of the genes on human chromosome 21. Previous microarray

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