Date of Thesis

Spring 2024

Description

Leishmaniasis is a parasitic disease spread by the bite of female sandflies and caused by over twenty species of protozoan parasites. The World Health Organization classifies leishmaniasis as a neglected tropical disease due to its prevalence in impoverished regions and the lack of research on developing better alternatives to current therapies. There is an urgent need to explore more effective treatment strategies since currently available treatments suffer from undesirable side effects due to drug toxicity and emerging drug resistant strains of Leishmania parasites. One possible approach to treating leishmaniasis involves disrupting an essential protein-protein interaction (PPI) in the parasite: the dimerization of ribose-5-phosphate isomerase B (RpiB). In this thesis, RpiB-binding peptides (RBPs) with two amino acid side chains linked via a hybrid coordination motif (HCM) are designed to bind the dimerization interface of RpiB to block formation of functional enzymes and result in parasitic death. RBPs equipped with an HCM coordinate a divalent metal ion of various identities (Co2+, Cu2+, Ni2+, Zn2+) and were hypothesized to induce an α-helical fold in the otherwise unstructured peptide to mimic the native structure of RpiB at the dimerization interface. Induction of α-helicity is advantageous because it is expected to confer properties favorable to a peptide therapeutic such as increased proteolytic stability, improved cellular internalization, and enhanced binding to a protein target. While circular dichroism data suggested that metal-bound RBPs were no more structured than their metal-free counterparts, analysis of the comparative proteolytic stabilities showed that some metal-bound RBPs had greater resistance to proteolytic cleavage.

Keywords

peptide, protein-protein interaction, leishmaniasis, metal binding

Access Type

Honors Thesis (Bucknell Access Only)

Degree Type

Bachelor of Science

Major

Cell Biology/Biochemistry

First Advisor

Sarah Smith

Available for download on Friday, April 30, 2027

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