Adaptation ofSaccharomyces cerevisiaeto the Herbicide 2,4-Dichlorophenoxyacetic Acid, Mediated by Msn2p- and Msn4p-Regulated Genes: Important Role ofSPI1

0303 health sciences Saccharomyces cerevisiae Proteins Glycosylphosphatidylinositols Herbicides Saccharomyces cerevisiae Adaptation, Physiological DNA-Binding Proteins 03 medical and health sciences Cell Wall Drug Resistance, Fungal Gene Expression Regulation, Fungal 2,4-Dichlorophenoxyacetic Acid Gene Deletion Heat-Shock Response Transcription Factors
DOI: 10.1128/aem.69.7.4019-4028.2003 Publication Date: 2003-07-02T22:00:09Z
ABSTRACT
ABSTRACT The possible roles of 13 Msn2p- and Msn4p-regulated genes in the adaptation Saccharomyces cerevisiae to herbicide 2,4- d -dichlorophenoxyacetic acid (2,4-D) were examined. Single deletion involved defense against oxidizing agents ( CTT1 , GRX1 GRX2/TTR1 ) or encoding chaperones HSP70 family SSA1 SSA4 SSE2 showed a slight effect. A more significant role was observed for heat shock HSP78 HSP26 HSP104 HSP12 HSP42 most which encode molecular chaperones. However, SPI1 gene, member glycosylphosphatidylinositol-anchored cell wall protein family, emerged as major determinant 2,4-D resistance. expression reduced loss viability an unadapted yeast population suddenly exposed herbicide, allowing earlier growth resumption. Significantly, involves rapid transient Msn4p-mediated activation (fivefold) S PI1 transcription. mRNA levels values slightly above those unstressed cells when adapted started duplication presence 2,4-D. Since leads higher β-1,3-glucanase sensitivity 2,4-D-stressed cells, it hypothesized that may involve Spi1p-mediated increase diffusional restriction liposoluble form across envelope. Such response would avoid futile cycle due reentry into counteracting active export anionic form, presumably through inducible plasma membrane transporter(s). Consistent with this concept, concentration 14 C-labeled 2,4-D-energized Δ spi1 mutant consequent intracellular acidification are than wild-type cells.
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