Cell wall perturbation in yeast results in dual phosphorylation of the Slt2/Mpk1 MAP kinase and in an Slt2-mediated increase in FKS2–lacZ expression, glucanase resistance and thermotolerance

Nobel, Hans de; Ruiz, César; Martı́n, Humberto; Morris, Wayne L.; Brul, Stanley; Molina, Marı́a; Klis, Frans M.

doi:10.1099/00221287-146-9-2121

Cited by 251 publications

(302 citation statements)

References 51 publications

(49 reference statements)

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“…Movement of Fks1p driven by actin is required for the construction of a uniform and solid cell wall (Utsugi et al, 2002). Transcription of FKS2 is up-regulated in response to cell wall stress induced by heat, cell wall mutations, and cell wall-perturbing agents (Zhao et al, 1998;de Nobel et al, 2000;Lagorce et al, 2003;Garcia et al, 2004). Deletion of KRE5 leads to a 114-fold up-regulation of FKS2 in response to an impaired cell wall (Kapteyn et al, 1999).…”

Section: Discussionmentioning

confidence: 99%

“…The yeast cell wall is an essential organelle that determines the shape and preserves the osmotic integrity of the cell by counteracting the internal turgor pressure. Mutants with weakened cell walls tend to form swollen cells with more spherical appearance and larger cell size than the wild-type (Popolo et al, 1993;de Nobel et al, 2000). The yeast cell wall has a two-layered structure.…”

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confidence: 99%

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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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Section: Discussionmentioning

confidence: 99%

mentioning

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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“…It has been previously demonstrated by others that cell wall stress can trigger an increase in cross-linking between cell wall proteins via β-1,6-glucan to chitin (Kapteyn et al, 1997) and that a defective incorporation of β-1,3-glucan can lead to an increase in chitin and mannan content in the cell wall (de Nobel et al, 2000;Kapteyn et al, 2001;Yin et al, 2005). These results highlight the importance of glucans, together with chitin and mannoproteins, in preserving cell wall integrity.…”

Section: Discussionmentioning

confidence: 98%

“…The Pkc1p-mediated cell wall integrity signalling pathway (CWIP) is principally responsible for orchestrating changes in the cell wall periodically throughout the cell cycle, as well as in response to various forms of cell wall stress (Heinisch et al, 1999;Levin, 2005;Martin et al, 2005;Vilella et al, 2005). Cell wall perturbation results in the dual phosphorylation of the Slt2p/Mpk1p MAP kinase (de Nobel et al, 2000) and Slt2p dual-phosphorylation has been previously demonstrated in myo1 cells by Western blot assay (Nishihama et al, 2003;RiveraMolina, 2005). We observed a decrease in dualphospho-Slt2 in myo1pUBC4 strains that suggested a restoration of cell wall integrity.…”

Section: Discussionmentioning

confidence: 99%

Dosage rescue by UBC4 restores cell wall integrity in Saccharomyces cerevisiae lacking the myosin type II gene MYO1

Díaz-Blanco

Rodríguez‐Medina

2007

Yeast

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Myosin II is important for normal cytokinesis and cell wall maintenance in yeast cells. Myosin II-deficient (myo1 ) strains of the budding yeast Saccharomyces cerevisiae are hypersensitive to nikkomycin Z (NZ), a competitive inhibitor of chitin synthase III (Chs3p), a phenotype that is consistent with compromised cell wall integrity in this mutant. To explain this observation, we hypothesized that the absence of myosin type II will alter the normal levels of proteins that regulate cell wall integrity and that this deficiency can be overcome by the overexpression of their corresponding genes. We further hypothesized that such genes would restore normal (wild-type) NZ resistance. A haploid myo1 strain was transformed with a yeast pRS316-GAL1-cDNA expression library and the cells were positively selected with an inhibitory dose of NZ. We found that high expression of the ubiquitin-conjugating protein cDNA, UBC4, restores NZ resistance to myo1 cells. Downregulation of the cell wall stress pathway and changes in cell wall properties in these cells suggested that changes in cell wall architecture were induced by overexpression of UBC4. UBC4-dependent resistance to NZ in myo1 cells was not prevented by the proteasome inhibitor clasto-lactacystin-β-lactone and required the expression of the vacuolar protein sorting gene VPS4, suggesting that rescue of cell wall integrity involves sorting of ubiquitinated proteins to the PVC/LE-vacuole pathway. These results point to Ubc4p as an important enzyme in the process of cell wall remodelling in myo1 cells.

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“…Finally, agents that interfere with cell wall biogenesis, such as the chitin antagonist Calcofluor white (Ketela et al, 1999), Congo red, or zymolyase (de Nobel et al, 2000), also stimulate signalling. Activation of CWI signalling can be detected by measurement of Slt2p protein kinase activity , immunological detection of phosphorylated Slt2p (Martín et al, 2000;de Nobel et al, 2000) or by induction of transcriptional reporters (Zhao et al, 1998;Jung et al, 2002;Kuranda et al, 2006).…”

Section: Introductionmentioning

confidence: 99%

Dissecting the transcriptional activation function of the cell wall integrity MAP kinase

Kim

Cosano

Levin

et al. 2007

Yeast

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The cell wall integrity signalling MAP kinase of Saccharomyces cerevisiae, Slt2p/ Mpk1p, is activated in response to cell wall stress. Slt2 and its mammalian orthologue ERK5 are unusual among MAP kinases, in that they possess the ability to activate transcription of a GAL1-lacZ reporter when fused to the DNA-binding domain of the Gal4 transcription factor. In this study, we demonstrate that transcriptional activation of a Gal4-Slt2p fusion is responsive to cell wall stress and requires phosphorylation of Slt2p. We identify two neighbouring but separable transcription activation domains within the C-terminal half of Slt2p. Additionally, we present data suggesting that intramolecular interactions controlled by phosphorylation of Slt2p regulate the function of these domains, which are masked by the N-terminal catalytic domain under inactive conditions. Finally, we demonstrate that Slt2p self-associates, probably through a glutamine-rich region within the C-terminal half of the protein.

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Cell wall perturbation in yeast results in dual phosphorylation of the Slt2/Mpk1 MAP kinase and in an Slt2-mediated increase in FKS2–lacZ expression, glucanase resistance and thermotolerance

Cited by 251 publications

References 51 publications

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

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

Dosage rescue by UBC4 restores cell wall integrity in Saccharomyces cerevisiae lacking the myosin type II gene MYO1

Dissecting the transcriptional activation function of the cell wall integrity MAP kinase

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