Nikkomycin Z is a specific inhibitor of Saccharomyces cerevisiae chitin synthase isozyme Chs3 in vitro and in vivo

Gaughran, J P; Lai, M.O.; Kirsch, Donald R.; Silverman, Sanford J.

doi:10.1128/jb.176.18.5857-5860.1994

Cited by 145 publications

(105 citation statements)

References 31 publications

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“…These results indicate that in the K l p m r l A strain, the apparatus responsible for the synthesis and localized deposition of chitin is impaired. This is supported by the observation that the K l p m r l A strain was hypersensitive to Nikkomycin Z , a competitive inhibitor of the major chitin synthase, Chs3p (Gaughran et al, 1994). In fact, while the growth of the K .…”

Section: Klfmrl Is Involved In the Morphogenesis Of The Cell Wallsupporting

confidence: 64%

Inactivation of the KlPMR1 gene of Kluyveromyces lactis results in defective cell-wall morphogenesis

et al. 1999

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The P-type Ca2+-ATPases are the transporters responsible for calcium homeostasis in the cell compartments of eukaryotes. The KlPMR7 gene of KIuyveromyces lactis encodes a P-type Ca*+-ATPase, which is functionally and structurally homologous to Pmrl p of Saccharomyces cerevisiae, the calcium pump localized in the Golgi membranes. In this work, a novel involvement of KlPmrlp in cell-wall morphogenesis of K, lactis is reported. KlpmrIA cells exhibited the loss of outer-chain extension in the glycosylation of secreted proteins. The absence of KlPmrlp resulted in the accumulation of round, large cells with an abnormally thick cell wall, as revealed by transmission electron microscopy. The deletant strain also showed a delocalized deposition of chitin in the lateral cell wall accompanied by an unbalanced ratio of insoluble to soluble glucans. These morphological defects were accompanied by the presence of irregularly shaped nuclei and by a DNA content greater than 2n. Addition of I 0 mM Ca2+ to the medium of the KlpmrIA strain reversed the chitin-deposition impairment, recovered the alteration to the glucan ratio and restored a normal thickness of the cell wall. The mutant cells resumed wildtype size, shape and nuclear morphology but the DNA content indicated the persistence of defects in the co-ordination between DNA replication and cell division. The glycosylation defects were completely unaffected by the calcium supplement. These results indicate that calcium homeostasis controlled by KlPmrlp plays an important role in the cell-wall morphogenesis of K. lactis.

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Section: Klfmrl Is Involved In the Morphogenesis Of The Cell Wallsupporting

confidence: 64%

Inactivation of the KlPMR1 gene of Kluyveromyces lactis results in defective cell-wall morphogenesis

et al. 1999

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“…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). In contrast, the wild-type and suppressor mutant tolerated 1 mM Nikkomycin Z with no obvious loss of viability.…”

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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“…As a result, it is now thought that an increased understanding of plant-Micromonospora interactions could produce further biological control agents against pests and pathogens [154]. Another chitinase-inhibiting compound nikkomycin is one of the most potent chitin synthase inhibitors isolated [155] and was first obtained from a culture of Streptomyces tendae. Unlike trehazolin and allosamidin, nikkomycin is a nucleoside peptide and so the utilisation of both Streptomyces and Micromonospora could improve the control of insect pests via the production of both pseudo-saccharide and peptide-based biopesticides.…”

Section: Chitin Synthase Disruption By Pesticidesmentioning

confidence: 99%

A Review of the Applications of Chitin and Its Derivatives in Agriculture to Modify Plant-Microbial Interactions and Improve Crop Yields

2013

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Abstract:In recent decades, a greater knowledge of chitin chemistry, and the increased availability of chitin-containing waste materials from the seafood industry, have led to the testing and development of chitin-containing products for a wide variety of applications in the agriculture industry. A number of modes of action have been proposed for how chitin and its derivatives can improve crop yield. In addition to direct effects on plant nutrition and plant growth stimulation, chitin-derived products have also been shown to be toxic to plant pests and pathogens, induce plant defenses and stimulate the growth and activity of beneficial microbes. A repeating theme of the published studies is that chitin-based treatments augment and amplify the action of beneficial chitinolytic microbes. This article reviews the evidence for claims that chitin-based products can improve crop yields and the current understanding of the modes of action with a focus on plant-microbe interactions.

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Nikkomycin Z is a specific inhibitor of Saccharomyces cerevisiae chitin synthase isozyme Chs3 in vitro and in vivo

Cited by 145 publications

References 31 publications

Inactivation of the KlPMR1 gene of Kluyveromyces lactis results in defective cell-wall morphogenesis

Inactivation of the KlPMR1 gene of Kluyveromyces lactis results in defective cell-wall morphogenesis

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

A Review of the Applications of Chitin and Its Derivatives in Agriculture to Modify Plant-Microbial Interactions and Improve Crop Yields

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