To access this work you must either be on the Smith College campus OR have valid Smith login credentials.

On Campus users: To access this work if you are on campus please Select the Download button.

Off Campus users: To access this work from off campus, please select the Off-Campus button and enter your Smith username and password when prompted.

Non-Smith users: You may request this item through Interlibrary Loan at your own library.

Publication Date

2013

Document Type

Honors Project

Department

Biological Sciences

Keywords

Filariasis, Nematodes as carriers of disease, Nematodes-Genetics, Promoters (Genetics), Thioredoxin, Peroxidase, Lymphatic filariasis, Brugia malayi, Peroxidase-2

Abstract

Lymphatic filariasis (LF), one of the Neglected Tropical Diseases (NTDs), is a parasitic infection caused by three nematodes: Wuchereria bancrofti (Wb), Brugia malayi (Bm) and Brugia timori (Bt). Currently, LF afflicts 120 million people worldwide, and puts 1.3 billion people in 80 different countries at risk of infection (WHO, 2010). After years of infection in an individual, LF can develop and lead to debilitating conditions such as elephantiasis and hydroceles (Nelson, 1998). Along with these severe health impacts, LF is also accompanied with negative social, economic and psychological effects. Lu et al. first identified Onchocerca volvulus Tpx2 gene to be upregulated in the infective larval stage (L3) and therefore predicted TPX2 protein to be important for parasite protection (1998). Later, Ghosh et al. identified Bm TPX as a protein that parasites use as a protective measure against exogenous sources of reactive oxygen species (1998). Bm TPX2 is located at the surface of the worms where it is in a position to detoxify toxic oxygen and protect the parasite from damage (Saunders, 2000). However, the lack of information on Tpx2 gene regulation makes it difficult to fully understand this gene, and also limits our discovery of ways in which we can overcome the infective L3 stage of B. malayi. The purpose of this study is to identify important regulatory and core promoter domains of Bm Tpx2 promoter. The Bm Tpx2 promoter was successfully amplified and cloned into the mCherry-1 plasmid. A 30 bp replacement mutation strategy was developed to make mutations in the promoter. The effect of these mutations was studied by assessing the mCherry signal under a florescence microscope in gene reporter 4 constructs. Although the results obtained do not lead to firm conclusions yet, they do prompt further investigation.

Language

English

Comments

90 p. : ill. (some col.) Honors project-Smith College, 2013. Includes bibliographical references (p. 84-89)

Download

Smith Only:
Off Campus Download

Share

COinS