β‐1,6‐Glucan synthesis in <i>Saccharomyces cerevisiae</i>

Shahinian, Serge; Bussey, Howard

doi:10.1046/j.1365-2958.2000.01713.x

Cited by 163 publications

(161 citation statements)

References 103 publications

(147 reference statements)

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“…Up-regulation of these genes agrees with the recent demonstration that the hyperaccumulation of chitin in these mutants was due to an increase in the flux of the chitin pathway (55). This group also contains genes implicated in ␤-glucan and mannan synthesis, like FKS2, which encodes the minor ␤-1,3-glucan synthase catalytic subunit (6, 29, 68); KRE6 and KRE11, which are involved in the synthesis of ␤-1,6- glucan (46,47); and KTR2, encoding a mannosyltransferase (69), as well as genes (ECM4, ECM8, ECM27, YPS3, and DFG5 (70 -72)) whose role in the cell wall construction has been inferred from genetic studies. Interestingly enough, we also identify several genes, which code for proteins that have a structural role in the architecture of the cell wall.…”

Section: Global Expression Changes In Cell Wall Mutants Usingsupporting

confidence: 88%

Genome-wide Analysis of the Response to Cell Wall Mutations in the Yeast Saccharomyces cerevisiae

Lagorce

Hauser

Labourdette

et al. 2003

Journal of Biological Chemistry

241

280

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Perturbations of the yeast cell wall trigger a repair mechanism that reconfigures its molecular structure to preserve cell integrity. To investigate this mechanism, we compared the global gene expression in five mutant strains, each bearing a mutation (i.e. fks1, kre6, mnn9, gas1, and knr4 mutants) that affects in a different manner the cell wall construction. Altogether, 300 responsive genes were kept based on high stringency criteria during data processing. Functional classification of these differentially expressed genes showed a substantial subset of induced genes involved in cell wall construction and an enrichment of metabolic, energy generation, and cell defense categories, whereas families of genes belonging to transcription, protein synthesis, and cellular growth were underrepresented. Clustering methods isolated a single group of ϳ80 up-regulated genes that could be considered as the stereotypical transcriptional response of the cell wall compensatory mechanism. The in silico analysis of the DNA upstream region of these co-regulated genes revealed pairwise combinations of DNA-binding sites for transcriptional factors implicated in stress and heat shock responses (Msn2/4p and Hsf1p) with Rlm1p and Swi4p, two PKC1-regulated transcription factors involved in the activation genes related to cell wall biogenesis and G 1 /S transition. Moreover, this computational analysis also uncovered the 6-bp 5 -AGCCTC-3 CDRE (calcineurindependent response element) motif in 40% of the coregulated genes. This motif was recently shown to be the DNA binding site for Crz1p, the major effector of calcineurin-regulated gene expression in yeast. Taken altogether, the data presented here lead to the conclusion that the cell wall compensatory mechanism, as triggered by cell wall mutations, integrates three major regulatory systems: namely the PKC1-SLT2 mitogen-activated protein kinase-signaling module, the "global stress" response mediated by Msn2/4p, and the Ca 2؉ /calcineurindependent pathway. The relative importance of these regulatory systems in the cell wall compensatory mechanism is discussed.Yeast and fungi are surrounded by a cell wall that is a complex structure essential for maintenance of the cell shape, prevention of lysis, and protection against harmful environmental conditions. The yeast cell wall architecture has been determined in detail over the past decade (1). It is a layered structure that is composed of ␤-1,3-and ␤-1,6-glucan (50 -60% of the cell wall dry mass), mannoproteins (40 -50%), and chitin (2%). ␤-1,3-Glucan and chitin form a fibrillar network to which mannoproteins are anchored, mostly through ␤-1,6-glucan. Some cell wall proteins, like the PIR family, can be directly linked to ␤-1,3-glucan (reviewed in Ref.2). The cell wall is not a rigid structure, since it endures all of the changes that the cell undergoes during division, morphogenesis, and differentiation.To ensure continuous integrity of the wall in accordance with its plasticity, complex mechanisms must be operating, which need to be strictly ...

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Section: Global Expression Changes In Cell Wall Mutants Usingsupporting

confidence: 88%

Genome-wide Analysis of the Response to Cell Wall Mutations in the Yeast Saccharomyces cerevisiae

Lagorce

Hauser

Labourdette

et al. 2003

Journal of Biological Chemistry

241

280

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“…1C accounting for 2% of ␤-(1,6)-glucan corresponds to the contribution from the kre5-ts2 cells in the preinoculum that were not grown at restrictive temperature. (ii) Kre5p displays significant similarity with UDP-glucose glycosyltransferases and contains a highly conserved C terminus with a UDP-glucose putative binding site (7,8). Other arguments are, however, against the participation of Kre5p to the enzymatic catalysis of ␤-(1,6)-glucans.…”

Section: Discussionmentioning

confidence: 99%

Cell Wall β-(1,6)-Glucan of Saccharomyces cerevisiae

Aimanianda

Clavaud

Simenel

et al. 2009

Journal of Biological Chemistry

119

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Despite its essential role in the yeast cell wall, the exact composition of the ␤-(1,6)-glucan component is not well characterized. While solubilizing the cell wall alkali-insoluble fraction from a wild type strain of Saccharomyces cerevisiae using a recombinant ␤-(1,3)-glucanase followed by chromatographic characterization of the digest on an anion exchange column, we observed a soluble polymer that eluted at the end of the solvent gradient run. Further characterization indicated this soluble polymer to have a molecular mass of ϳ38 kDa and could be hydrolyzed only by ␤-(1,6)-glucanase. Gas chromatographymass spectrometry and NMR ( 1 H and 13 C) analyses confirmed it to be a ␤-(1,6)-glucan polymer with, on average, branching at every fifth residue with one or two ␤-(1,3)-linked glucose units in the side chain. This polymer peak was significantly reduced in the corresponding digests from mutants of the kre genes (kre9 and kre5) that are known to play a crucial role in the ␤-(1,6)-glucan biosynthesis. In the current study, we have developed a biochemical assay wherein incubation of UDP-[ 14 C]glucose with permeabilized S. cerevisiae yeasts resulted in the synthesis of a polymer chemically identical to the branched ␤-(1,6)-glucan isolated from the cell wall. Using this assay, parameters essential for ␤-(1,6)-glucan synthetic activity were defined.

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“…Restored ␤-1,3-glucan levels in pgs1⌬ mutant cells in the presence of the kre5 W1166X suppressor mutation (Table 2) could be mediated by up-regulation of FKS2 expression. In fact, increased ␤-1,3-glucan is a general characteristic shared by several kre mutants, along with defective ␤-1,6-glucan synthesis (Roemer et al, 1994;Dijkgraaf et al, 1996;Shahinian et al, 1998;Shahinian and Bussey, 2000).…”

Section: Discussionmentioning

confidence: 99%

Loss of Function ofKRE5Suppresses Temperature Sensitivity of Mutants Lacking Mitochondrial Anionic Lipids

Zhong

Gvozdenović-Jeremić

Webster

et al. 2005

MBoC

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Disruption of PGS1, which encodes the enzyme that catalyzes the committed step of cardiolipin (CL) synthesis, results in loss of the mitochondrial anionic phospholipids phosphatidylglycerol (PG) and CL. The pgs1⌬ mutant exhibits severe growth defects at 37°C. To understand the essential functions of mitochondrial anionic lipids at elevated temperatures, we isolated suppressors of pgs1⌬ that grew at 37°C. One of the suppressors has a loss of function mutation in KRE5, which is involved in cell wall biogenesis. The cell wall of pgs1⌬ contained markedly reduced ␤-1,3-glucan, which was restored in the suppressor. Stabilization of the cell wall with osmotic support alleviated the cell wall defects of pgs1⌬ and suppressed the temperature sensitivity of all CL-deficient mutants. Evidence is presented suggesting that the previously reported inability of pgs1⌬ to grow in the presence of ethidium bromide was due to defective cell wall integrity, not from "petite lethality." These findings demonstrated that mitochondrial anionic lipids are required for cellular functions that are essential in cell wall biogenesis, the maintenance of cell integrity, and survival at elevated temperature. INTRODUCTIONCardiolipin (CL), a unique anionic phospholipid with dimeric structure, is ubiquitous in eukaryotes and primarily found in the mitochondrial inner membrane . CL plays a key role in mitochondrial bioenergetics (Jiang et al., 2000; Greenberg, 2000, 2002;Schlame et al., 2000;Pfeiffer et al., 2003) and is also involved in mitochondrial biogenesis (Kawasaki et al., 1999;Jiang et al., 2000). Defective remodeling of CL is associated with Barth syndrome, a severe genetic disorder characterized by cardiomyopathy, neutropenia, skeletal myopathy, and respiratory chain defects (Vreken et al., 2000). The phenotype of Barth syndrome is dependent upon multiple factors that are not well understood (Barth et al., 1983(Barth et al., , 1996. Elucidation of the functions of CL will help to clarify the abnormalities associated with this disorder.The biosynthesis of CL is conserved in eukaryotic organisms. It occurs via three enzymatic reactions , including formation of phosphatidylglycerolphosphate (PGP) from CDP-DAG and glycerol-3-P, dephosphorylation of PGP to phosphatidylglycerol (PG), and condensation of CDP-DAG and PG to form CL. Disruption of PGS1, the structural gene encoding PGP synthase, results in the complete loss of both PG and CL (Janitor et al., 1996;Chang et al., 1998a). The crd1⌬ mutant, which lacks CL synthase, has no detectable CL but accumulates PG (Jiang et al., 1997;Chang et al., 1998b;Tuller et al., 1998;Jiang et al., 2000;Pfeiffer et al., 2003;Zhong et al., 2004). The human taffazin gene (TAZ1), which is associated with Barth syndrome, encodes a transacylase that may be involved in the remodeling of CL (Xu et al., 2003). Deletion of the yeast homolog of this gene, TAZ1, leads to decreased CL, aberrant CL acyl species, and accumulation of monolysocardiolipin . Mutants deficient in CL biosynthesis exhibit growth defects at elevat...

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β‐1,6‐Glucan synthesis in Saccharomyces cerevisiae

Cited by 163 publications

References 103 publications

Genome-wide Analysis of the Response to Cell Wall Mutations in the Yeast Saccharomyces cerevisiae

Genome-wide Analysis of the Response to Cell Wall Mutations in the Yeast Saccharomyces cerevisiae

Cell Wall β-(1,6)-Glucan of Saccharomyces cerevisiae

Loss of Function ofKRE5Suppresses Temperature Sensitivity of Mutants Lacking Mitochondrial Anionic Lipids

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