NDLI: Networks of genes modulating the pleiotropic drug response in Saccharomyces cerevisiae.

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Networks of genes modulating the pleiotropic drug response in Saccharomyces cerevisiae.

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	Yibmantasiri, Ploi Bircham, Peter W. Maass, David R. Bellows, David S. Atkinson, Paul H.
Description	Country affiliation: New Zealand Author Affiliation: Yibmantasiri P ( School of Biological Sciences, Victoria University of Wellington, Room 321, MacDiarmid Building, Kelburn, Wellington, 6012, New Zealand. Paul.Atkinson@vuw.ac.nz.)
Abstract	The pleiotropic drug response (PDR) or multidrug resistance (MDR) are cellular defence mechanisms present in all species to deal with potential toxicity from environmental small molecule toxins or bioactives. The rapid induction of MDR by xenobiotics in mammalian cells and PDR in budding yeast (S. cerevisiae) has been well studied but how pathway specificity is achieved across different structural classes of xenobiotics is not well understood. As a novel approach to this problem we investigated the genome-wide network of genes modulating the yeast PDR. Fluorescently-tagged ABC pumps Pdr5p-GFP and Yor1p-GFP were used as real-time reporters for the Pdr1p/Pdr3p controlled response. Using the yeast non-essential gene deletion set fifty-four gene deletions that suppressed up-regulation of reporter fluorescence to the cell surface in the presence of atorvastatin were identified by high content confocal automated microscopy. Secondary validation using spot dilution assays to known PDR substrates and Western blot assays of Pdr5p expression confirmed 26 genes able to modulate the PDR phenotype. By analysis of network connectivity, an additional 10 genes that fell below the primary screen cut-off were predicted to be involved in PDR and confirmed as above. The PDR modulating genes taken together were enriched in signalling (Rho-GTPase, MAPK), Mediator complexes, and chromatin modification (subunits of ADA and SAGA complexes). Many of the gene deletions cause extra sensitivity in Δpdr1Δpdr3 strains strongly suggesting that there are alternative pathways to upregulate PDR, independently of Pdr1p/Pdr3p. We present here the first high-content microscopy screening for PDR modulators, and identify genes that are previously unsuspected regulators of PDR apparently contributing via network interactions.
File Format	HTM / HTML
ISSN	1742206X
Issue Number	1
Volume Number	10
e-ISSN	17422051
Journal	Molecular BioSystems
Language	English
Publisher	Royal Society of Chemistry
Publisher Date	2014-01-01
Publisher Place	Great Britain (UK)
Access Restriction	Subscribed
Subject Keyword	Discipline Molecular Biology Discipline Biochemistry Drug Resistance, Multiple Genetics Gene Regulatory Networks Saccharomyces Cerevisiae Proteins Biosynthesis Signal Transduction Atp-binding Cassette Transporters Metabolism Atorvastatin Calcium Dna-binding Proteins Gene Deletion Gene Expression Regulation, Fungal Drug Effects Heptanoic Acids Pharmacology Pyrroles Saccharomyces Cerevisiae Transcription Factors Transcription, Genetic Journal Article Research Support, Non-u.s. Gov't
Content Type	Text
Resource Type	Article
Subject	Molecular Biology Biotechnology

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