Snf1 Dependent Destruction of Med13 is Required for Programmed Cell Death Following Oxidative Stress in Yeast

Abstract

All eukaryotic cells, when faced with unfavorable environmental conditions, have to decide whether to mount a survival or cell death response. The conserved cyclin C and its kinase partner Cdk8 play a key role in this decision. Both are members of the Cdk8 kinase module that, along with Med12 and Med13, associate with the core mediator complex of RNA polymerase II. In S. cerevisiae, oxidative stress triggers Med13 destruction1, which thereafter releases cyclin Ci nto the cytoplasm. Cytoplasmic cyclin C associates with mitochondria where it induces hyper-fragmentation and programmed cell death2. This suggests a model in which oxidative stress mediated destruction o fMed13 represents a key molecular switch which commits the cell to programmed cell death. Thus it is important to decipher the precise molecular mechanisms that control Med13 destruction following exposure to oxidative stress

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Rowan University

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oai:rdw.rowan.edu:som_facpub-1126Last time updated on 4/24/2020View original full text link

This paper was published in Rowan University.

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