Methylmercury (MeHg) is an environmental contaminate that has harmful effects on
wildlife. Anthropogenic sources like coal mining emit inorganic mercury (Hg) into the
atmosphere. From the atmosphere, Hg is deposited into aquatic ecosystems. Once in aquatic
ecosystems, inorganic Hg is converted to MeHg by bacteria and enters the food web. Emergent
aquatic insects (e.g. dragonflies), insects with aquatic larval stages and terrestrial adult stages,
will transport MeHg from the aquatic ecosystem to terrestrial predators like songbirds.
This project focuses on MeHg contamination of nestling Red-winged blackbirds
(Agelaius phoeniceus) from nests at the Eagle Mountain Hatchery Pond Facility. It is believed
that nestling Red-winged blackbirds (RWBL) consume aquatic-based prey, primarily odonates
(damselflies and dragonflies) but can consume terrestrial prey as well. Odonates are known to
have high levels of MeHg contamination. Although studies have attempted to observe what
RWBL parents feed nestlings, there are no studies of the actual prey composition in the
nestlings’ digestive tracts. Insects consumed by birds can be analyzed because external coverings
of insect body parts (head capsules, mandibles, legs) are composed of undigestible chiton. This study looks at nestling RWBL diets to quantify odonates in their diets. We will sort through varying fecal samples from the Pond Facility in order to determine the diet composition of the RWBL, and if the composition correlates with MeHg levels in nestlings.

In many patients with breast cancer, a mutation in their BRCA1 gene disrupts BRCA1 protein’s function as a tumor suppressor. One mechanism through which BRCA1 prevents cancer is by acting as an enzyme to attach a signaling protein called ubiquitin to a H2A, a DNA packaging protein. This attachment inhibits gene expression of DNA damaging proteins. Here, we determine whether enzymatic activity of BRCA1 towards H2A is a conserved feature in C. elegans, a microscopic worm used as a model organism.

To measure conservation, we used mutagenesis to introduce mutations into C. elegans’ BRCA1 at a region homologous to the known human H2A binding site. Similar to mutations at this site in human BRCA1, our results showed a decrease in enzymatic activity when mutations were present. This indicates that C. elegans BRCA1 and human BRCA1 use similar mechanisms of attachment to H2A. To develop tools to study this reaction in C. elegans, we need to understand the position on H2A to which ubiquitin is attached. To accomplish this, we generated C. elegans H2A using cloning to eventually determine the specific location of ubiquitin attachment.

Our experiment is about diabetes and Human and synthetic insulin crystallization in a microgravity environment. This experiment is designed to help us find out if there is a way to prevent crystallization of insulin, especially if we understand how it happens in microgravity. When insulin crystallizes, the bacteria that usually makes it viable stops working. This would cause it to be ineffective for patients in dire need of this medication. To complete this experiment we would like to send three different varieties of insulin in a type 3 mini lab FME (Fluids Mixture Enclosure) to the International Space Station (ISS), kept in ambient temperatures, to see if it crystallization occurs within a certain amount of time. We will keep the experiment refrigerated at or below 40℉ during transportation to the ISS and again after arrival back to our lab to prevent crystallization occurring outside of the experiment. Refrigeration slows the crystallization growth and this is how it is stored on Earth. Keeping our experiment refrigerated during transportation is an important step because the insulin crystallization growth should only be measured while in microgravity. It is also important to note that crystallization of insulin is slow so change in crystal growth will not be evident if out of refrigeration for short periods of time. We would like to keep our insulin types out of refrigeration for a period of six weeks minimum. While testing insulin crystallization in microgravity, we will be conducting the same experiment on Earth as our control. If we can understand more about synthetic insulin, maybe one day diabetic men and women can follow their passion of being astronauts and humans with this disease will have the opportunity to go to microgravity environments for extended periods of time.

Hepatitis C virus currently infects around 130-170 million people. HCV, a member of the Flaviviridae family, causes chronic liver inflammation which can lead to liver cirrhosis or hepatocellular carcinoma. One of the nonstructural proteins of HCV, NS5A, is known to diminish the host innate immune response via inhibition of antiviral gene expression. NS5A blocks NFkB from entering the nucleus, decreasing transcription of IFN-B. Specifically, NS5A 10A, a mutant form of the protein, is known to greatly diminish the activity of the IFN B promoter. Our goal is to determine how WT NS5A and another mutant, NS5A H27, affect this pathway as well. We did this by transfecting HEK 293 cells with the NS5A mutant of interest, infecting the cells with Sendai virus, and subsequently measuring the activity of the IFN B promoter using a luciferase assay. In addition, NS5A contains three domains: I, II, and III. We are interested in determining which domain of NS5A is particularly important for blocking antiviral gene expression. We designed primers to created truncations of the protein containing the individual domains via PCR.

Previous studies showed that exposures to thyroid inhibitors during early stages of development lead to long-lasting alterations in disease resistance. Therefore, the goal of this project was to assess the effects of early life stages thyroid disruption on the maturation and function of immune cells using propylthiouracil (PTU)-exposed fathead minnow as a model system. The specific objectives of this study were to evaluate the impacts of early life stage PTU-exposure on 1) neutrophil migration and 2) transcriptomic markers of lymphoid and myeloid cell development. These objectives were accomplished by exposing fathead minnow embryos to 35 mg/L and 70 mg/L PTU for 10 days, while evaluating neutrophils migration with a tail nicking assay and assessing immune cell development by measuring transcriptomic markers of maturation at 10 days post fertilization (dpf). There were no differences in transcriptomic markers for lymphoid cell development between PTU and control groups. However, PTU-exposed larvae showed a decreased amount of neutrophils at wound site as well as decreased v-ymb expression compared to those of the control at days 7 and 10, indicating that early life stage thyroid disruption interfered with the normal development and subsequently reduced immune response in these organisms.