Grant: Doctoral Research Award: Canada Graduate Scholarships

Mitochondria are known as "powerhouses of the cell," making the energy needed to run our cells along with many other important roles. However, in a busy cell environment, mitochondria often face high demands and stress. If this is not dealt with, damaged and dysfunctional mitochondria can cause diseases which affect parts of our bodies with high energy use, such as our brain, muscles, heart, or can even contribute to cancer. Sometimes mitochondria need help to keep working at peak condition. Mitochondria can alert the nucleus (the "control centre" of the cell) to start producing proteins that help mitochondria survive stress and regain function. I want to understand how stressed mitochondria communicate with the nucleus. We study mitochondria in yeast cells because they share many similarities to human cells. Our lab has found that when mitochondria are stressed, a protein called Mge1 enters the nucleus. Mge1 activates (or "turns on") another protein called Pdr3. When Pdr3 is "on," it directs the cell to make proteins that help mitochondria deal with stress. Thus, we can think of Mge1 as a messenger between the mitochondria and the nucleus. However, we still don't understand exactly how Mge1 tells the nucleus what to do. To understand this, I will study how Mge1 enters the nucleus when mitochondria are stressed and how Mge1 activates Pdr3. Active Pdr3 also turns on a pathway which allows cells to remove toxins, called multidrug resistance. Multidrug resistance helps infectious yeast species to survive antifungals which are used to treat yeast infections. I will also study Mge1 and Pdr3 from infectious yeast species, to understand how mitochondrial stress may cause yeast treatment resistance. Through this work, I hope to improve our understanding of diseases involving dysfunctional mitochondria, as well as processes leading to antifungal resistant yeast infections, which may help us develop new ways to treat yeast infections.