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Undergraduate Research Project Management System

Copper Homeostatis: Histone Modification at the CUP1 Locus

Status Current
Seeking Researchers No
Start Date 09/01/2008
End Date 06/30/2009
Funding Source Alaska Heart Institute Fellowships
Funding Amount
Community Partner
Related Course
Last Updated 07/05/2008 01:25AM
Keywords

People

Faculty
  Jocelyn Krebs

Student Researchers
  Cody Rall

Abstract

Cells maintain copper at specific levels because it is essential for many biochemical processes, yet toxic at high amounts. Copper homeostasis is maintained through various mechanisms that either uptake copper from the environment or sequester/export it from the cell. Genetic defects in copper homeostasis result in serious diseases in humans, including Menkes disease and Wilson's disease. In the presence of high copper levels, the yeast Saccharomyces cerevisiae immediately expresses the CUP1 gene to produce the Cup1 metallothionein protein, which binds to excess copper within minutes of exposure. The CUP1 gene is then rapidly shut down within 30 minutes of copper exposure. Histone modifications, particularly acetylation, play a major role in controlling gene expression in all eukaryotes. I will investigate the pattern and function of histone modifications that coordinate this precise gene regulation, in order to understand the mechanisms controlling CUP1 activation and shutdown. I will also investigate histone acetylation patterns that may control expression of RUF5, an anti-sense RNA expressed from the complementary strand of CUP1. Finally, I will identify the enzymes responsible for these histone modification patterns.

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