Regulation of copper homeostasis and programmed cell death by a key Drosophila ubiquitination pathway.

Our cells must carefully regulate their exposure to the heavy metal copper. Too little copper starves enzymes which rely on it to function, while too much copper is a potent cellular poison and can induce cell death. We do not yet understand how our cells can sense copper levels and balance its essentiality with its toxicity. This thesis explores how the enzyme UbcD1 may act as a ‘copper thermostat,’ helping cells assess and respond to dynamic changes in copper concentrations by regulating both copper transport and cellular stress responses by transcription factors such as p53.