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2022 Award Finalist Lena Pernas, PhD.
Lena Pernas received her bachelor’s degree from UCLA and Ph.D. from Stanford University. There, she worked with John Boothroyd to eludicate how mitochondria and the human parasite Toxoplasma gondii physically interact, and how chronic toxoplasmosis affects human immune responses. After receiving her Ph.D., Lena joined the lab of Dr. Luca Scorrano at the University of Padua where she studied how mitochondria counteract microbes. Her lab at the Max Planck Institute for Biology of Ageing is interested in the mechanisms by which an infected cell actively rewires metabolic processes and organellar function to defend against the challenge of microbial infection, and how human metabolism affects disease progression.
Synopsis of research
To generate energy, mitochondria consume nutrients that invading microbes depend on. This competing interest predicts an inverse relationship between mitochondrial health and microbial fitness. Although several pathogens disrupt host mitochondrial function, it was unknown whether mitochondria act to impede pathogen replication.
As a PhD student in the lab of Dr. John Boothroyd, I identified the molecule that enable mitochondria to recognize and bind to the human parasite Toxoplasma gondii, which infects ~1/3 of the world’s human population. The dramatic changes I observed in mitochondrial shape during Toxoplasma infection led me to ask if mitochondria actively defend cells against microbes (contrary to the dogma that mitochondria are targets for microbes)? To address this question, I moved to the mitochondrial biology unit of Dr. Luca Scorrano where I discovered that host mitochondria act as nutrient competitors to Toxoplasma, and limit the parasite’s growth by restricting its access to host lipids. This work showed that mitochondrial metabolism functions as an innate immune-type defense and sheds light on how we can harness metabolism to develop anti-microbial therapies.
Synopsis of research
To generate energy, mitochondria consume nutrients that invading microbes depend on. This competing interest predicts an inverse relationship between mitochondrial health and microbial fitness. Although several pathogens disrupt host mitochondrial function, it was unknown whether mitochondria act to impede pathogen replication.
As a PhD student in the lab of Dr. John Boothroyd, I identified the molecule that enable mitochondria to recognize and bind to the human parasite Toxoplasma gondii, which infects ~1/3 of the world’s human population. The dramatic changes I observed in mitochondrial shape during Toxoplasma infection led me to ask if mitochondria actively defend cells against microbes (contrary to the dogma that mitochondria are targets for microbes)? To address this question, I moved to the mitochondrial biology unit of Dr. Luca Scorrano where I discovered that host mitochondria act as nutrient competitors to Toxoplasma, and limit the parasite’s growth by restricting its access to host lipids. This work showed that mitochondrial metabolism functions as an innate immune-type defense and sheds light on how we can harness metabolism to develop anti-microbial therapies.
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