Major
Molecular Biology
Anticipated Graduation Year
2025
Access Type
Restricted Access
Abstract
The oxidizing environment in the mosquito midgut poses a challenge for the malaria parasite Plasmodium. To protect itself, the parasite employs antioxidant strategies, such as the glutathione (GSH) and thioredoxin (Trx) systems. Here, we present our first differential gene expression analysis of Trx- and GSH-associated genes between knockout Plasmodium berghei with a disrupted GSH system and wild-type parasites in the asexual blood stages and mosquito-stage ookinete cultures. Our findings suggest that compensation by the thioredoxin system may not be sufficient or does not occur, highlighting the central role of the GSH system in the development and survival of Plasmodium.
Community Partners
University of Puerto Rico
Faculty Mentors & Instructors
Samantha R. Webster, Master's Student, Department of Biology at Loyola Univerisity Chicago; Stefan M. Kanzok, Associate Professor, Biology Department at Loyola University Chicago
Supported By
Adelfa E. Serrano, Professor, University of Puerto Rico School of Medicine;
Creative Commons License
This work is licensed under a Creative Commons Attribution-Noncommercial-No Derivative Works 3.0 License.
Investigating the Glutathione-Dependent Mechanism of Mosquito Infection by Malaria Parasite Plasmodium
The oxidizing environment in the mosquito midgut poses a challenge for the malaria parasite Plasmodium. To protect itself, the parasite employs antioxidant strategies, such as the glutathione (GSH) and thioredoxin (Trx) systems. Here, we present our first differential gene expression analysis of Trx- and GSH-associated genes between knockout Plasmodium berghei with a disrupted GSH system and wild-type parasites in the asexual blood stages and mosquito-stage ookinete cultures. Our findings suggest that compensation by the thioredoxin system may not be sufficient or does not occur, highlighting the central role of the GSH system in the development and survival of Plasmodium.