Analysis of gene network regulating yeast multidrug resistance by artificial activation of transcription factors: Involvement of Pdr3 in salt tolerance

Miyuki Onda, Kazuhisa Ota, Tomoko Chiba, Yoshiyuki Sakaki, Takashi Ito

Research output: Contribution to journalArticle

21 Citations (Scopus)

Abstract

We established a strategy to constitutively activate Zn2Cys 6-type protein by fusing its DNA-binding domain with the VP16 trans-activation domain. To explore gene network regulating yeast multidrug resistance, the strategy was applied to Pdr1, Pdr3 and Yrr1, known to regulate multidrug resistance, as well as three uncharacterized Yrr1-related transcription factors. DNA microarray analysis revealed that all of the six mutants induce typical drug transporter genes including SNQ2 and YOR1, suggesting redundancy in regulation. On the other hand, each displays a unique spectrum of targets, which is coincident with the phylogenetic tree of the transcription factors and presumably reflects their functional specification. Indeed, careful analysis of target genes specific to each transcription factor led us to reveal an unexpected role for Pdr3 in salt tolerance. The strategy would thus contribute not only to identify target genes but to reveal redundancy and specificity in complex gene regulatory networks.

Original languageEnglish
Pages (from-to)51-59
Number of pages9
JournalGene
Volume332
Issue number1-2
DOIs
Publication statusPublished - May 12 2004
Externally publishedYes

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Salt-Tolerance
Gene Regulatory Networks
Multiple Drug Resistance
Transcription Factors
Yeasts
Genes
Microarray Analysis
Oligonucleotide Array Sequence Analysis
DNA
Pharmaceutical Preparations
Proteins

All Science Journal Classification (ASJC) codes

  • Genetics

Cite this

Analysis of gene network regulating yeast multidrug resistance by artificial activation of transcription factors : Involvement of Pdr3 in salt tolerance. / Onda, Miyuki; Ota, Kazuhisa; Chiba, Tomoko; Sakaki, Yoshiyuki; Ito, Takashi.

In: Gene, Vol. 332, No. 1-2, 12.05.2004, p. 51-59.

Research output: Contribution to journalArticle

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