In low- and middle-income countries (LMICs), human exposure to animals can represent a significant source of enteropathogens. The presence of domestic and non-domestic animals either in the vicinity or in immediate households within LMICs have the potential to contaminate soil and high-touch surfaces leading to enteropathogen transmission and infection. Among LMICs, access to water, sanitation, and hygiene (WASH) is limited and is responsible for contributing to the global disease burden. Lack of WASH regulations and implementation can compound transmission and infection rates of enteropathogens from animal exposures. The objective of this study is to determine the sources and quantities of household animal fecal contamination, an important exposure pathway for enteropathogens, in Ecuadorian households. Quantitative PCR (qPCR) assays were used to identify host-associated fecal contamination by detecting gene fragments of gut microbes that are specific to the feces of a given human or animal host. These microbial source tracking (MST) marker assays were used on environmental samples collected in Ecuador households including floor, mother and child hand rinses, and domestic water to assess the abundance and sources of household fecal contamination. MST marker targets included human feces associated markers (HF183 & HumM2), dog feces makers (DG37), ruminant feces markers (Rum2Bac), pig feces markers (Pic2Bac), bird droppings markers (GFD), and general bacteroidales markers (GenBac). The anticipated results are that the qPCR data will continue to indicate high levels of general and human-associated animal fecal contamination in animal-owning Ecuadorian households as previously observed in Phase 2 of this study. Findings from this study will highlight the need for the development and implementation of relevant public health interventions aimed at reducing animal exposures and improving overall hygiene practices to decrease the global disease burden among LMICs.

Cells communicate with each other and their environment via signaling pathways. When a cell receives a signal, it is processed by several proteins. Oftentimes, the same proteins are used by multiple pathways that process distinct signals and produce distinct cellular outputs. I am investigating how the cell is able to correctly process signals using Wnt signaling as a model pathway. Wnt signaling helps regulate cell growth and differentiation and is therefore tightly associated with many diseases. Both Wnt and insulin signaling processing utilize the enzyme glycogen synthase kinase 3β (GSK3β). Activation of insulin signaling results in the phosphorylation of GKS3β. However, if phosphorylated GSK3β from insulin signaling interacts with Wnt proteins, Wnt signaling can be inappropriately activated in the absence of a Wnt signal. The mechanism by which cells prevent improper activation of Wnt signaling is unknown. I am researching the role scaffold proteins play in signaling pathway insulation. Traditionally, scaffold proteins facilitate reactions by binding enzymes and their substrates, bringing them in close proximity to each other. It has also been shown that scaffold proteins can assist in promoting chemical reactions through mechanisms other than binding. Because the scaffold protein Axin binds GSK3β as well as PP2A, an enzyme that dephosphorylates GSK3β, I propose that Axin promotes insulation of the Wnt pathway. Using in vivo human cell culture assays, I have determined that Axin promotes dephosphorylation of GSK3β by PP2A through a mechanism more complex than bringing the two proteins in close proximity with each other. I will use in vitro kinetic assays to determine the underlying kinetic mechanism of this effect. Determining the kinetics of scaffold-mediated insulation will produce a model that can be applied to other signaling pathways and is important in understanding how to specifically target Wnt signaling for disease treatment without affecting other pathways.