Abstract. Social dispersal in primate populations provide benefits such as increased mating opportunities while reducing the chances of inbreeding and resource competition in the newly dispersed location. However, social dispersal also brings significant costs due to a higher risk of mortality while dispersing. Thus, social dispersal is a critical process shaping the demography of populations yet, very little is known about the factors influencing dispersal in primate populations. Here we aim to identify the drivers of social dispersal in Cayo Santiago male rhesus macaques by quantifying their effect on the probability of annual social group migrations. Cayo Santiago males show multiple dispersal events throughout their lives. On average, males disperse from their natal group at 4.91 years of age (SE=1.75), whereas throughout their adult lives they dispersed at a mean age of 8.64 years (SE=0.01). We will test whether age, group size, and the number of dispersal groups available explain annual dispersal probability using generalized linear mixed effects models. Our analysis will be based on individual level longitudinal data expanding 45 years from 1973 to 2017. We predict that dispersal will peak at puberty and will show a negative association with age thereafter, whereas the number of available groups and group density will display a positive association with dispersal probability. Understanding dispersal decisions is critical to address the demography of primate populations as dispersal influences survival and reproduction.

Alzheimer’s disease (AD) is a neurodegenerative disease that eventually leads to a loss of basic human brain function. The disease manifests itself through the destruction of nerve cells. The amyloid beta fragment (A-Beta-42) that results from the cleavage of the amyloid precursor protein (APP), forms plaques in the brain which causes cell death. The fruit fly Drosophila melanogaster has a protein APP-like (APPL) that shares a high degree of conservation to human APP. Therefore, we plan to use powerful genetic tools and tractable neuroanatomy available in Drosophila to study human APP and its homolog APPL. We will test APPL mutants, as well as flies expressing transgenes of different variants of APPL and human APP. A flight behavioral assay will be used to analyze the effects of the expression of the different transgenes in flies that are 2 days (2d), 10 days (10d), and 30 days old (30d). To test the flies, a drop test will be conducted which consists of dropping flies in a graduated cylinder and recording their landing distance. The measured flight performance will be a reading of the function of the motor network including identified flight motoneurons. The observations that will be recorded will help provide better understanding of the function of APP and APPL.

Autophagy is the process in which the cell rids itself of damaged organelles and other materials in an effort to recycle macromolecules. The formation of autophagosomes, double-membraned vesicles, is a crucial step in autophagy and is dependent on the expression of autophagy-related gene (ATG) Atg9. This protein is known to be important in regulating autophagosome formation and was first discovered in yeast, but more complex eukaryotes have evolved to have two separate homologs of Atg9: Atg9a and Atg9b. However, few studies have studied the differences between the two homologs. Our lab has found that Atg9a and Atg9b may play distinct roles in general autophagy and mitophagy, selective autophagy of the mitochondria, in the heart. We observed that vesicles containing Atg9a localize near the mitochondria in neonatal cardiomyocytes and that Atg9a is degraded upon induction of mitophagy. However, in the absence of Atg9a, Atg9b is similarly degraded during mitophagy. Our findings suggest that Atg9a plays a more specific role in mitophagy while Atg9b functions mainly in general autophagy. We will investigate the degradation of Atg9a and Atg9b in response to other autophagy - and mitophagy-inducing stimuli, including rapamycin, oligomycin and antimycin, and starvation. We hypothesize that Atg9a and Atg9b are degraded during mitophagy and general autophagy respectively to prevent excessive formation of autophagosomes.

Problems in antifungals Within the realm of medicine, one growing concern is the overuse of current treatments and the eventual consequence of antibiotics and antifungal to stop working.Within my research, I explore what types of antifungal compounds clinicians have available as well as why we are limited in treatment options for fungal infections. Some of the topics covered will be the toxicity of current fungicides, infections resulting rom opportunistic fungus in immune-compromised individuals, and the mechanics of synthesizing new compounds. In the experimental phase, I plan on testing compounds Oklahoma states chemistry department made in house that have displayed antifungal activity. I will be testing these compounds against popular species of fungi that are responsible for such infections such as C.albicaba .in this experiment I will also be comparing the compounds against popular antifungal flucanizol . Then later in the experiment phase, I will be testing said an anti-fungal combination against collected fungi culture from cystic fibrosis patients who are a vulnerable community concerning fungal infections.