Specific effects of triarimol on sterol biosynthesis in Ustilago maydis

Ragsdale, Nancy

doi:10.1016/0005-2760(75)90047-8

Cited by 133 publications

(51 citation statements)

References 24 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…No treatment or mutation affected the amounts or the proportions of major phospholipids in plasma membranes of U. maydis (Table 5 ) . This is in accordance with previous studies where, although triarimol or propiconazole had severe effects on the sterol compostition of U. maydis or Taphrina deformans, respectively, no effect was observed in the corresponding phospholipid fractions (Ragsdale, 1975 ;Weete et al, 1985).…”

Section: Phospholipidssupporting

confidence: 93%

See 1 more Smart Citation

Fungicides and sterol-deficient mutants of Ustilago maydis: plasma membrane physico-chemical characteristics do not explain growth inhibition

et al. 1997

View full text Add to dashboard Cite

Plasma membrane vesicles from erg1 I and erg2 sterol-deficient mutants and from wild-type Ustilago maydis sporidia treated with and without inhibitors of sterol 14a-demethylase or sterol A8-A7 isomerase (triadimenol and fenpropimorph fungicides, respectively) were purified by aqueous two-phase partitioning. Changes in plasma membrane lipid composition were mostly restricted to sterols and complex lipid-bound fatty acids (CLB fatty acids). There was a greater accumulation of abnormal sterols (14a-methyl-or A8-unsaturated sterols) in plasma membranes from sterol-def icient mutants than from those treated with their fungicide counterparts. However, greater growth inhibition was observed on fungicide-treated wild-type than on mutants. Changes in CLB fatty acids were restricted to alterations in the relative proportion of linoleic acid (18:2) with respect to oleic acid (18: 1). The 18:2 to 18:l ratio found in CLB fatty acids in plasma membranes could be correlated to rates of sporidial growth but not to accumulation of a particular abnormal sterol or to the extent of sterol replacement. Plasma membrane permeability to protons was increased moderately in the mutants only. No changes were observed in plasma membrane fluidity. Plasma membrane H+-ATPase activity was increased up to twofold in those cases with lower growth rate. It was concluded that fungiciddnduced growth inhibition in U. maydis was not due to accumulation of abnormal sterols in plasma membranes but probably due to intracellular ATP depletion by the H+-ATPase and that changes in 18:2 to 18: 1 ratio in CLB fatty acids were not directly dependent on the plasma membrane physical state or lipid composition but were possibly part of a stress adaptation mechanism.

show abstract

Section: Phospholipidssupporting

confidence: 93%

“…Similar changes in plasma membrane CLB fatty acids have been reported in U. maydis in response to triarimol (an azole antifungal; Ragsdale, 1975), in Candida albicans treated with 0.1 pM ketoconazole (Vanden Bossche, 1993) and in 7'. deformans treated with propiconazole (Weete et al, 1985(Weete et al, , 1991.…”

Section: Fatty Acidssupporting

confidence: 68%

Fungicides and sterol-deficient mutants of Ustilago maydis: plasma membrane physico-chemical characteristics do not explain growth inhibition

et al. 1997

View full text Add to dashboard Cite

show abstract

“…The sterols of the amphotericin B-resistant mutants were identified by comparison with data in the literature (Ragsdale, 1975 ;Walsh & Sisler, 1982). RRt and mass spectral data for all these sterols are presented in Table 1.…”

Section: Analysis Of Sterols Accumulating In Wild-type U Maydis Strmentioning

confidence: 99%

“…These sterols also accumulate in U . maydis sporidia treated with C-14 sterol demethylase inhibitors (Ragsdale & Sisler, 1972;Ragsdale, 1975), and in the U. maydis Erg40 mutant (Walsh & Sisler, 1982). No further analyses of these isolates was done since this type of mutant had previously been isolated and characterized in detail (Walsh & Sisler, 1982).…”

Section: Analysis Of Sterols Accumulating In Wild-type U Maydis Strmentioning

confidence: 99%

Isolation and characterization of polyene-resistant mutants from the maize smut pathogen, Ustilago maydis, defective in ergosterol biosynthesis

James

Burden

Loeffler

et al. 1992

Journal of General Microbiology

View full text Add to dashboard Cite

Ustilago maydis mutants resistant to polyene antibiotics were screened for defects in ergosterol biosynthesis. Slowgrowing mutants recovered after selecting for amphotericin B resistance were devoid of ergosterol and accumulated the methylated sterols, 14a-methylfecosterol, obtusifoliol and eburid, indicating that these isolates were impaired in C-14 sterol demethylation and were similar to the Erg40 mutant of U. m y & By contrast, nystatin-and pimaricin-resistant isolates which exhibited reduced growth rates showed a dysfunction in C-8 sterol isomerization. In these mutants (Erg2) ergosterol was replaced by the A*-sterols, ergosta-5,8,22-trienol, ergosta-8,22-dienol, fecosterol and ergost-8-enol. Analysis of a random sample of polyene-resistant isolates that grew normally revealed that although most retained a typical wild-type sterol profile, two of the isolates failed to accumulate ergosterol. The msjor sterols detected in these isolates were ergosta-7,22-dienol and ergosta-7-eno1, suggesting a lesion in C-5 sterol desaturation in these mutants (Erg3). Of four Erg2 mutants recovered, one mutant, selected on nystatin, contained low but detectable amounts of ergosterol. Ergosterol was not detected immediately after selection in the three other pimaricin-resistant Erg2 mutants. Although the growth of three of the Erg2 mutants remained unchanged during non-selective culture, one mutant reverted and began to grow at a greater rate than the rest; analysis of the sterols produced by this strain revealed that ergosterol was now present, but at lower concentrations than those in the wild-type strain. No changes in the type of sterol formed were observed in the other slower-growing Erg2 mutants even after prolonged culture. All the Erg2 mutants exhibited morphological abnormalities; sporidia were swollen and distorted, and the inability of sporidia to separate after cell division led to the development of highly branched, multicellular groups of cells.

show abstract

“…Inhibitors were added as methanolic solutions so that the methanol did not exceed 1% in the culture media. After centrifugation from culture media, sporidia were lyophilized, and crude lipids were extracted with chloroform-methanol (2:1, vol/vol) (11,18,20 Sterols of unsaponified lipid samples were analyzed by gas-liquid chromitography after separation by TLC, whereas saponified lipid smples were analyzed directly. Analyses were performed on a Glowall Chromalab 310 chromatograph by using a coluimn (1.8 m by 3.4 mm) packed with 3% SE-30 on Gas Chrom Q (100 to 120 mesh) at 255°C.…”

mentioning

confidence: 99%

Effects of Miconazole and Dodecylimidazole on Sterol Biosynthesis in Ustilago maydis

Henry

Sisler

1979

Antimicrob Agents Chemother

View full text Add to dashboard Cite

Miconazole at minimal fungitoxic concentrations inhibits ergosterol biosynthesis in sporidia of Ustilago maydis by interference with sterol C14 demethylation. The action is analogous to that of the fungicides tiarimol and fenariniol. The fungicide 1-dodecylimidazole at low concentrations (0.1 to 0.25 yg/ml) inhibits sterol C14 demethylation; however, at higher concentrations (1.0 ug/ml or greater) it also inhibits 2,3-oxidosqualene cyclization and subsequent tranamethylation. It is postulated that this diversity of effects of 1-dodecylimidazole results from binding of the inhibitor to sterol carrier protein(s).Miconazole is a fungitoxic agent with a wide antifungal spectrum used medically to control mycotic infections (27). Various observations with Candida albicans after exposure times ranging from 3 to 24 h indicated that miconazole affects membrane permeability and transport as well as cell morphology (8-10, 26, 28).In studies with imazalil, a miconazole analog, Van Tuyl observed that cross-resistance invariably occured between the fonner compound and fenarimol in mutants of Aspergillus nidulans (30,31). Fenarimol, like triarimol, is an inhibitor of ergosterol biosynthesis (3, 19). These results suggested that the mode of action of miconazole was possibly analogous to that of the sterol C14 demethylation inhibitors triarimol (18,21), fenarimol, imazalil (16,24), triadimefon (2), triforine (23), and Denmert (14). Recent studies show, in fact, that miconazole is an inhibitor of ergosterol biosynthesis in Ustilago maydis (12) and C. albicans (29).N-dodecylimidazole, like miconazole, is a fungitoxic 1-alkylimidazole. This compound is reported to inhibit cholesterol biosynthesis in rat livers (K. H. Baggaley, R. M. Hindley, J. L. Tee, and G. S. Brooks, British Patent 1,364,312, January 1971). Atkin et al. concluded that it is a specific inhibitor of 2,3-oxidosqualene cyclase, the enzyme which converts 2,3-oxidosqualene to lanosterol (1). It was of interest to compare the effects of these two inhibitors on the sterol biosynthetic pathway in U. mnaydis, an organism in which the action of triarimol has been thoroughly investigated (12,18,20,21). This report presents the results of these investigations.MATERIALS AND METHODS Sporidia of U. maydis (DC) Cda. ATCC 14826 were cultured as previously described (5,20), in a defined nutrient medium at an initial concentration of 6.9 x 106 sporidia per ml (0.2 mg [dry Wvt] per ml). Inhibitors were added as methanolic solutions so that the methanol did not exceed 1% in the culture media. After centrifugation from culture media, sporidia were lyophilized, and crude lipids were extracted with chloroform-methanol (2:1, vol/vol) (11,18,20 Sterols of unsaponified lipid samples were analyzed by gas-liquid chromitography after separation by TLC, whereas saponified lipid smples were analyzed directly. Analyses were performed on a Glowall Chromalab 310 chromatograph by using a coluimn (1.8 m by 3.4 mm) packed with 3% SE-30 on Gas Chrom Q (100 to 120 mesh) at 255°C. Compounds were detecte...

show abstract

Specific effects of triarimol on sterol biosynthesis in Ustilago maydis

Cited by 133 publications

References 24 publications

Fungicides and sterol-deficient mutants of Ustilago maydis: plasma membrane physico-chemical characteristics do not explain growth inhibition

Fungicides and sterol-deficient mutants of Ustilago maydis: plasma membrane physico-chemical characteristics do not explain growth inhibition

Isolation and characterization of polyene-resistant mutants from the maize smut pathogen, Ustilago maydis, defective in ergosterol biosynthesis

Effects of Miconazole and Dodecylimidazole on Sterol Biosynthesis in Ustilago maydis

Contact Info

Product

Resources

About