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  Interfering with Glycolysis Causes Sir2-Dependent Hyper-Recombination of Saccharomyces cerevisiae Plasmids.

Ralser, M., Zeidler, U., & Lehrach, H. (2009). Interfering with Glycolysis Causes Sir2-Dependent Hyper-Recombination of Saccharomyces cerevisiae Plasmids. PLoS ONE, 4(4), e5376-e5376. doi:doi:10.1371/journal.pone.0005376.

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Item Permalink: http://hdl.handle.net/11858/00-001M-0000-0010-7DA8-0 Version Permalink: http://hdl.handle.net/11858/00-001M-0000-0010-7DA9-E
Genre: Journal Article
Alternative Title : PLOS ONE

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 Creators:
Ralser, Markus1, Author              
Zeidler, Ute, Author
Lehrach, Hans1, Author              
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1Dept. of Vertebrate Genomics (Head: Hans Lehrach), Max Planck Institute for Molecular Genetics, Max Planck Society, ou_1433550              

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 Abstract: Glyceraldehyde-3-phosphate dehydrogenase (GAPDH) is a key metabolic regulator implicated in a variety of cellular processes. It functions as a glycolytic enzyme, a protein kinase, and a metabolic switch under oxidative stress. Its enzymatic inactivation causes a major shift in the primary carbohydrate flux. Furthermore, the protein is implicated in regulating transcription, ER-to-Golgi transport, and apoptosis. We found that Saccharomyces cerevisiae cells null for all GAPDH paralogues (Tdh1, Tdh2, and Tdh3) survived the counter-selection of a GAPDH–encoding plasmid when the NAD+ metabolizing deacetylase Sir2 was overexpressed. This phenotype required a fully functional copy of SIR2 and resulted from hyper-recombination between S. cerevisiae plasmids. In the wild-type background, GAPDH overexpression increased the plasmid recombination rate in a growth-condition dependent manner. We conclude that GAPDH influences yeast episome stability via Sir2 and propose a model for the interplay of Sir2, GAPDH, and the glycolytic flux.

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Language(s): eng - English
 Dates: 2009-04-24
 Publication Status: Published in print
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Title: PLoS ONE
  Alternative Title : PLOS ONE
Source Genre: Journal
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Pages: - Volume / Issue: 4 (4) Sequence Number: - Start / End Page: e5376 - e5376 Identifier: ISSN: 1932-6203