Our project focuses on discovering how collagen becomes defective in Ehlers-Danlos Syndrome (EDS).  Research indicates that the gene AEBP1 encodes Aortic Carboxypeptidase-Like Protein (ACLP), which associates with collagen in the Extracellular Matrix and has roles in development, tissue repair, fibrosis and overall structural integrity of tissue. Variants in AEBP1 have been associated with EDS, which causes  joint laxity, hypermobility, abnormal wound healing, and hyperextensible skin. ACLP enhances collagen polymerization and binds to several types of collagens through its discoidin domain. We hypothesize that EDS patients will have lower levels of ACLP and this is the source of the defective collagen, which is driving EDS disease progression. Our study will seek to advance EDS research through the creation of a biosensor that expresses the antibody for ACLP as well as Green Fluorescent Protein (GFP) in order to quantify the levels of ACLP in joint tissues of both healthy patients and patients with EDS. Due to the complex nature of the folding needed to express the fusion protein, we utilize the eukaryotic chassis (Pichia pastoris). This is a methylotrophic yeast that is commonly used for high-level expression of recombinant proteins, including full-length antibodies, in place of the traditional E. coli. chassis.