Yeast 1,3-β-Glucan Synthase Activity Is Inhibited by Phytosphingosine Localized to the Endoplasmic Reticulum

Abe, Mitsuhiro; Nishida, Ikuo; Minemura, Masayo; Qadota, Hiroshi; Seyama, Yousuke; Watanabe, T.; Ohya, Yoshikazu

doi:10.1074/jbc.m102179200

Cited by 32 publications

(20 citation statements)

References 52 publications

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“…From these results, it is thought that the induction of -1,6-glucan synthesis genes is an attempt to improve resistance to AFB 1 , though this interpretation does not agree with EXG2. FEN1, which relates to -1,3-glucan synthesis [36], was also repressed by AFB 1 (Table 4). Therefore, it is thought that an abnormal cell wall can be easily generated.…”

Section: Defective Ptc1 Causes Dysfunction Of Cell Wall Gene Expressimentioning

confidence: 99%

Gene expression profile of MAP kinase PTC1 mutant exposed to Aflatoxin B1: dysfunctions of gene expression in glucose utilization and sphingolipid metabolism

Suzuki

Iwahashi

2009

CBIJ

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Aflatoxin B 1 (AFB 1 ) is a harmful and cancer-causing mycotoxin generated by Aspergillus flavus. Its mechanism of toxicity has not been fully clarified and further research is required. In this study, we attempted to further clarify aflatoxin B 1 toxicity using the results of S. cerevisiae gene expression analysis. In a Ser/Thr phosphatase 2C disruptant (ptc1Δ) with weakened activity of anti-toxic components (cell wall and membrane), the addition of low concentrations of sodium dodecyl sulfate resulted in elevated susceptibility to AFB 1 . From the microarray results, expression changes in DNA synthesis or repair, sphingolipid metabolism, glucose metabolism, and cell wall-related genes were well detected. Our results indicate that AFB 1 causes sphingolipid metabolism disorder, leading to dysfunction in signal secretion and inhibition of efficient glucose metabolism, which supplies the materials for cell wall proteins and cellular components, resulting in repression of the stress response to external toxicants.

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Section: Defective Ptc1 Causes Dysfunction Of Cell Wall Gene Expressimentioning

confidence: 99%

Gene expression profile of MAP kinase PTC1 mutant exposed to Aflatoxin B1: dysfunctions of gene expression in glucose utilization and sphingolipid metabolism

Suzuki

Iwahashi

2009

CBIJ

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“…Fks1 is localized to the plasma membrane at sites of polarized growth and cell wall remodeling throughout the cell cycle, and this localization coincides with that of actin patches (Qadota et al 1996;Dijkgraaf et al 2002;Utsugi et al 2002). Fks1 transits the secretory pathway because it accumulates intracellularly in vesicular transport mutants and its activity is sensitive to phytosphingosine levels in the ER (El-Sherbeini and Clemas 1995; Abe et al 2001;File S7).…”

Section: Biosynthesis Of Wall Components At the Plasma Membranementioning

confidence: 99%

Architecture and Biosynthesis of the Saccharomyces cerevisiae Cell Wall

2012

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The wall gives a Saccharomyces cerevisiae cell its osmotic integrity; defines cell shape during budding growth, mating, sporulation, and pseudohypha formation; and presents adhesive glycoproteins to other yeast cells. The wall consists of b1,3-and b1,6-glucans, a small amount of chitin, and many different proteins that may bear N-and O-linked glycans and a glycolipid anchor. These components become cross-linked in various ways to form higher-order complexes. Wall composition and degree of cross-linking vary during growth and development and change in response to cell wall stress. This article reviews wall biogenesis in vegetative cells, covering the structure of wall components and how they are cross-linked; the biosynthesis of N-and O-linked glycans, glycosylphosphatidylinositol membrane anchors, b1,3-and b1,6-linked glucans, and chitin; the reactions that cross-link wall components; and the possible functions of enzymatic and nonenzymatic cell wall proteins. TABLE OF CONTENTS Abstract 775Introduction 777

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“…FEN1 is a long-chain fatty acid elongase. Mutants in FEN1 exhibit defects in budding and sporulation, likely due to altered membrane phospholipid content (27). SPO7 is dispensable for mitosis but is required for premeiotic DNA synthesis, a normal mutation rate, recombination, meiosis I and II, glycogen degradation, and sporulation.…”

Section: Characteristics Most Useful In Predicting Ssl Interactionsmentioning

confidence: 99%

Combining biological networks to predict genetic interactions

Wong

Zhang

Tong

et al. 2004

Proc. Natl. Acad. Sci. U.S.A.

229

226

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Genetic interactions define overlapping functions and compensatory pathways. In particular, synthetic sick or lethal (SSL) genetic interactions are important for understanding how an organism tolerates random mutation, i.e., genetic robustness. Comprehensive identification of SSL relationships remains far from complete in any organism, because mapping these networks is highly labor intensive. The ability to predict SSL interactions, however, could efficiently guide further SSL discovery. Toward this end, we predicted pairs of SSL genes in Saccharomyces cerevisiae by using probabilistic decision trees to integrate multiple types of data, including localization, mRNA expression, physical interaction, protein function, and characteristics of network topology. Experimental evidence demonstrated the reliability of this strategy, which, when extended to human SSL interactions, may prove valuable in discovering drug targets for cancer therapy and in identifying genes responsible for multigenic diseases.

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Yeast 1,3-β-Glucan Synthase Activity Is Inhibited by Phytosphingosine Localized to the Endoplasmic Reticulum

Cited by 32 publications

References 52 publications

Gene expression profile of MAP kinase PTC1 mutant exposed to Aflatoxin B1: dysfunctions of gene expression in glucose utilization and sphingolipid metabolism

Gene expression profile of MAP kinase PTC1 mutant exposed to Aflatoxin B1: dysfunctions of gene expression in glucose utilization and sphingolipid metabolism

Architecture and Biosynthesis of the Saccharomyces cerevisiae Cell Wall

Combining biological networks to predict genetic interactions

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