Chitin synthase III: Synthetic lethal mutants and “stress related” chitin synthesis that bypasses the
            <i>CSD3/CHS6</i>
            localization pathway

Osmond, Barbara C.; Specht, Charles A.; Robbins, Phillips W.

doi:10.1073/pnas.96.20.11206

Cited by 63 publications

(62 citation statements)

References 57 publications

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“…The data may imply that Sed1p plays an important role in the progression of the cell cycle through M phase by locating at or near the bud neck, which is consistent with the recent report by Caro et al (1998) that SED1 expression was enhanced in late M phase. Recently, Osmond et al (1999) reported that a double mutant of mnn9 and chs3 (chitin synthetase III) was lethal and that Figure 4. FACS analysis of R210 (pGAL-SED1).…”

Section: Discussionmentioning

confidence: 99%

Cooperative functions of the mannoprotein‐encoding genes in the biogenesis and maintenance of the cell wall in Saccharomyces cerevisiae

Horie

Isono

2001

Yeast

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To elucidate the roles of genes involved in the cell wall biogenesis and function in Saccharomyces cerevisiae, we isolated and characterized mutants that were lethal in a strain in which the SED1 gene encoding a cell wall mannoprotein was disrupted. Thus, double mutants of SED1 and either MNN9 or MNN10 were unable to grow and YOL155c on a multicopy plasmid could suppress their synthetic lethality. A Yol155cp-GFP fusion protein was found to localize to the cell wall, suggesting that it might also be a cell wall mannoprotein. Subsequently, we analysed the effects of the shut-off of SED1 in a sed1 and mnn9 double mutant: cells after the shut-off showed anomalous cellular morphology and died in the mitotic M phase. From these and other results, we postulate that these genes function cooperatively with each other and in a cell cycle-dependent manner in the biogenesis and maintenance of cell wall in S. cerevisiae.

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Section: Discussionmentioning

confidence: 99%

Cooperative functions of the mannoprotein‐encoding genes in the biogenesis and maintenance of the cell wall in Saccharomyces cerevisiae

Horie

Isono

2001

Yeast

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“…In pgs1⌬ and suppressor mutants, however, chitin staining was uniformly distributed to the lateral cell wall, and the bud scar was hardly distinguishable from the rest of the cell wall. Hyperaccumulation of chitin in cell wall mutants is mediated by chitin synthase III (CSIII) (Osmond et al, 1999;Valdivieso et al, 2000). When grown in the presence of 0.1 mM Nikkomycin Z, a known inhibitor of CSIII (Gaughran et al, 1994), viability of the pgs1⌬ mutant was reduced by 40% (our unpublished data).…”

Section: Disruption Of Pgs1 Leads To a Defective Cell Wallmentioning

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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“…The amount of chitin in the cell wall of the mating projection is drastically increased, and instead of a welldefined ring a diffuse ring is seen at the base of the mating projection (see Orlean, 1997). Responsible for this deposition of chitin is Chs3p, the chitin synthase involved in synthesis of the chitin ring and the chitin in the lateral wall, as well as the chitin synthesis in response to cell wall damage (Osmond et al, 1999 ;Garcia-Rodriguez et al, 2000). However, neither Chs3p nor Chs4p is essential for cell fusion.…”

Section: Matingmentioning

confidence: 99%

Differential regulation of cell wall biogenesis during growth and development in yeast

2001

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Chitin synthase III: Synthetic lethal mutants and “stress related” chitin synthesis that bypasses the CSD3/CHS6 localization pathway

Cited by 63 publications

References 57 publications

Cooperative functions of the mannoprotein‐encoding genes in the biogenesis and maintenance of the cell wall in Saccharomyces cerevisiae

Cooperative functions of the mannoprotein‐encoding genes in the biogenesis and maintenance of the cell wall in Saccharomyces cerevisiae

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

Differential regulation of cell wall biogenesis during growth and development in yeast

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