Kristin D. Lane, Ph.D.

Summary: Multidrug resistant (MDR) pathogens are a global threat and a challenge for modern medicine. As MDR pathogens outpace the development of new therapeutics, it is critical to develop alternative treatment strategies. The Lane Lab studies Plasmodium falciparum parasites, which cause malaria in humans, and kills almost a half-million people annually, creating a desperate need for new interventions.

In the human malaria parasite, Plasmodium falciparum, mitochondrial function is critically essential in both the human and mosquito life stages. Despite being a validated drug target for decades, most mitochondrial proteins and pathways remain uncharacterized. The lack of knowledge regarding basic functions and their regulation creates an enormous gap in our ability to exploit mitochondrial biology and biochemistry for targeted drug development. It is challenging to Investigate the malaria parasite mitochondrial components. There is only a single mitochondrion per parasite for most of the life cycle. The multicopy genomes are linear or circular, encode three essential electron transport chain (ETC) genes, but no tRNAs for translation. Thus, the parasite mitochondrion has evolved noncanonical means of gene expression and regulation compared to other eukaryotes.

Minimum classes: N/A

Projects: INBRE students can participate in many different aspects of ongoing projects in my laboratory, including: 1) Genetic editing of Plasmodium falciparum membrane proteins to facilitate separation of fluorescent organelles to determine the proteome of the mitochondria and apicoplast (a parasite-specific organelle). 2) Building a targeted DNA exonuclease to degrade linear DNA fragments in the parasite mitochondria 3) Analysis of the proteome dataset to identify proteins involved in gene expression of the mitochondrial genes.

Projects 1 and 2 will use standard molecular biology techniques (PCR, DNA isolation, restriction enzyme analysis, gel electrophoresis, etc) to build plasmids used for CRISPR/Cas9 editing membrane protein genes to be fluorescent. Project 3 will not be available until after summer 2025.