Transcript – Molecular Mechanisms of Intracellular Copper Trafficking

Hello, my name is Michelle Gohil, and I will talk about our funded research project focused on identifying genetic regulators of mitochondrial copper homeostasis. So, what if it’s well known that mitochondria start co-operative, middle aged Cytochrome C oxidase? The terminal enzyme of the mitochondria is producing how copper is delivered to mitochondria is not well understood. To identify genetic irregularities of mitochondria, copper homeostasis, we performed a DNA barczyk based genome wide screen using yeast deletion mutations, which identified a number of known regulators of mitochondria, copper homeostasis. A follow up study on some of the top hits led to a discovery of Apte three complex, which showed that EP three is required for the maintenance of mitochondrial circumciser oxidase, as well as a regular B.H. Similar analysis identified that the immigrants are also required for maintaining regular insider activity. So, our work connected vacuolar ph with mitochondrial copper homeostasis. And we found that by restoring VOECKLER in these mutants, arbitrary and remote, we could rescue Cytochrome Xerox’s activity consistent with this genetic data we found at pharmacological inhibition of regular ETPs. Also, results introduced mitochondrial copper inside of this abundance and activity. So, this work led to an interesting new discovery that mitochondrial copper homeostasis is regulated by vascular function.