Journal article
Retrograde regulation of multidrug resistance in Saccharomyces cerevisiae
Gene, Vol.354(1-2), pp.15-21
2005
DOI: 10.1016/j.gene.2005.03.019
PMID: 15896930
Abstract
Communication between the mitochondria and the nucleus is essential to ensure correct metabolic coordination of the cell. Signaling pathways leading from the mitochondria to the nucleus are referred to as retrograde signaling and were first discovered in the yeast
Saccharomyces cerevisiae. Cells that lack their mitochondrial genome (ρ
0 cells) trigger expression of the nuclear
CIT2 gene in order to ensure adequate amino acid biosynthesis. More recently, it has been found that a different set of genes involved in multidrug resistance in
S.
cerevisiae is strongly induced in ρ
0 cells. During a search for negative regulators of the ATP-binding cassette (ABC) transporter-encoding gene
PDR5, it was observed that ρ
0 mutants exhibited dramatic up-regulation of the transcript of this gene. This induction was due to the post-translational activation of a direct upstream regulator of
PDR5 that was designated Pdr3p. Loss of the
LGE1 gene led to a block in ρ
0-mediated induction of
PDR5 expression. Lge1p has been observed by others to be involved in histone H2B ubiquitination along with the ubiquitin-conjugating enzyme Rad6p and the ubiquitin ligase Bre1p. Our studies provide evidence that Lge1p has another function unique from H2B ubiquitination that is required for retrograde regulation of
PDR5 transcription. We have also found that the Pdr pathway regulates expression of several genes involved in sphingolipid biosynthesis. These findings suggest that the physiological role of the
PDR genes might be to regulate membrane homeostasis and ρ
0-triggered changes in this parameter may be the signal controlling
PDR gene expression.
Details
- Title: Subtitle
- Retrograde regulation of multidrug resistance in Saccharomyces cerevisiae
- Creators
- W.S. Moye-Rowley - University of Iowa
- Resource Type
- Journal article
- Publication Details
- Gene, Vol.354(1-2), pp.15-21
- Publisher
- Elsevier B.V
- DOI
- 10.1016/j.gene.2005.03.019
- PMID
- 15896930
- ISSN
- 0378-1119
- eISSN
- 1879-0038
- Language
- English
- Date published
- 2005
- Academic Unit
- Molecular Physiology and Biophysics; Internal Medicine
- Record Identifier
- 9984297502102771
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