Tryptophan confers resistance to SDS-associated cell membrane stress in Saccharomyces cerevisiae.

Sodium dodecyl sulfate is a detergent that disrupts cell membranes, activates cell wall integrity signaling and restricts cell growth in Saccharomyces cerevisiae. However, the underlying mechanism of how sodium dodecyl sulfate inhibits cell growth is not fully understood. Previously, we have shown t...

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Main Authors: Lea Schroeder, Amy E Ikui
Format: Article
Language:English
Published: Public Library of Science (PLoS) 2019-01-01
Series:PLoS ONE
Online Access:https://doi.org/10.1371/journal.pone.0199484
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spelling doaj-5f19c29c345540ef8d01d401bb414a592021-03-03T20:49:46ZengPublic Library of Science (PLoS)PLoS ONE1932-62032019-01-01143e019948410.1371/journal.pone.0199484Tryptophan confers resistance to SDS-associated cell membrane stress in Saccharomyces cerevisiae.Lea SchroederAmy E IkuiSodium dodecyl sulfate is a detergent that disrupts cell membranes, activates cell wall integrity signaling and restricts cell growth in Saccharomyces cerevisiae. However, the underlying mechanism of how sodium dodecyl sulfate inhibits cell growth is not fully understood. Previously, we have shown that deletion of the MCK1 gene leads to sensitivity to sodium dodecyl sulfate; thus, we implemented a suppressor gene screening revealing that the overexpression of TAT2 tryptophan permease rescues cell growth in sodium dodecyl sulfate-treated Δmck1 cells. Therefore, we questioned the involvement of tryptophan in the response to sodium dodecyl sulfate treatment. In this work, we show that trp1-1 cells have a disadvantage in the response to sodium dodecyl sulfate compared to auxotrophy for adenine, histidine, leucine or uracil when cells are grown on rich media. While also critical in the response to tea tree oil, TRP1 does not avert growth inhibition due to other cell wall/membrane perturbations that activate cell wall integrity signaling such as Calcofluor White, Congo Red or heat stress. This implicates a distinction from the cell wall integrity pathway and suggests specificity to membrane stress as opposed to cell wall stress. We discovered that tyrosine biosynthesis is also essential upon sodium dodecyl sulfate perturbation whereas phenylalanine biosynthesis appears dispensable. Finally, we observe enhanced tryptophan import within minutes upon exposure to sodium dodecyl sulfate indicating that these cells are not starved for tryptophan. In summary, we conclude that internal concentration of tryptophan and tyrosine makes cells more resistant to detergent such as sodium dodecyl sulfate.https://doi.org/10.1371/journal.pone.0199484
collection DOAJ
language English
format Article
sources DOAJ
author Lea Schroeder
Amy E Ikui
spellingShingle Lea Schroeder
Amy E Ikui
Tryptophan confers resistance to SDS-associated cell membrane stress in Saccharomyces cerevisiae.
PLoS ONE
author_facet Lea Schroeder
Amy E Ikui
author_sort Lea Schroeder
title Tryptophan confers resistance to SDS-associated cell membrane stress in Saccharomyces cerevisiae.
title_short Tryptophan confers resistance to SDS-associated cell membrane stress in Saccharomyces cerevisiae.
title_full Tryptophan confers resistance to SDS-associated cell membrane stress in Saccharomyces cerevisiae.
title_fullStr Tryptophan confers resistance to SDS-associated cell membrane stress in Saccharomyces cerevisiae.
title_full_unstemmed Tryptophan confers resistance to SDS-associated cell membrane stress in Saccharomyces cerevisiae.
title_sort tryptophan confers resistance to sds-associated cell membrane stress in saccharomyces cerevisiae.
publisher Public Library of Science (PLoS)
series PLoS ONE
issn 1932-6203
publishDate 2019-01-01
description Sodium dodecyl sulfate is a detergent that disrupts cell membranes, activates cell wall integrity signaling and restricts cell growth in Saccharomyces cerevisiae. However, the underlying mechanism of how sodium dodecyl sulfate inhibits cell growth is not fully understood. Previously, we have shown that deletion of the MCK1 gene leads to sensitivity to sodium dodecyl sulfate; thus, we implemented a suppressor gene screening revealing that the overexpression of TAT2 tryptophan permease rescues cell growth in sodium dodecyl sulfate-treated Δmck1 cells. Therefore, we questioned the involvement of tryptophan in the response to sodium dodecyl sulfate treatment. In this work, we show that trp1-1 cells have a disadvantage in the response to sodium dodecyl sulfate compared to auxotrophy for adenine, histidine, leucine or uracil when cells are grown on rich media. While also critical in the response to tea tree oil, TRP1 does not avert growth inhibition due to other cell wall/membrane perturbations that activate cell wall integrity signaling such as Calcofluor White, Congo Red or heat stress. This implicates a distinction from the cell wall integrity pathway and suggests specificity to membrane stress as opposed to cell wall stress. We discovered that tyrosine biosynthesis is also essential upon sodium dodecyl sulfate perturbation whereas phenylalanine biosynthesis appears dispensable. Finally, we observe enhanced tryptophan import within minutes upon exposure to sodium dodecyl sulfate indicating that these cells are not starved for tryptophan. In summary, we conclude that internal concentration of tryptophan and tyrosine makes cells more resistant to detergent such as sodium dodecyl sulfate.
url https://doi.org/10.1371/journal.pone.0199484
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AT amyeikui tryptophanconfersresistancetosdsassociatedcellmembranestressinsaccharomycescerevisiae
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