Involvement of the alternative oxidase in cellular energy production in the wheat ‘take all’ fungus, Gaeumannomyces graminis var tritici

Joseph‐Horne, Tim; Wood, Paul M.; Heppner, Claudia; Hollomon, D. W.

doi:10.1002/(sici)1096-9063(199903)55:3<367::aid-ps911>3.3.co;2-5

Cited by 4 publications

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“…Alternative respiration in response to the inhibition of cytochrome pathway has been described in Septoria tritici (Mycosphaerella graminicola) as a second potential mechanism of resistance to respiratory inhibitors acting at the Qo site of cytochrome bc 1 complex (Ziogas et al, 1997). This potential bypass of target site of strobilurin fungicides has also been described in other plant pathogens such as M. grisea (Yukioka et al, 1997) Gaeumannomyces graminis (Joseph-Horne et al, 1999), B. cinerea (Tamura et al, 1999) and V. inaequalis (Olaya and Ko¨ller, 1999a). However, the alternative respiration pathway is essential for fungal metabolism but probably not for field resistance to QoIs (Ziogas et al, 1997;Olaya and Ko¨ller, 1999b).…”

Section: Discussionmentioning

confidence: 99%

Characterization of Laboratory Mutants of Botrytis cinerea Resistant to QoI Fungicides

et al. 2006

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Mutants of Botrytis cinerea with moderate and high resistance to pyraclostrobin, a Qo inhibitor of mitochondrial electron transport at the cytochrome bc 1 complex, were isolated at a high mutation frequency, after nitrosoguanidine mutagenesis and selection on medium containing pyraclostrobin and salicylhydroxamate (SHAM), a specific inhibitor of cyanide-resistant (alternative) respiration. Oxygen uptake in whole cells was strongly inhibited in the wild-type strain by pyraclostrobin and SHAM, but not in the mutant isolates. Cross-resistance studies with other Qo and Qi inhibitors (QoIs and QiIs) of cytochrome bc 1 complex of mitochondrial respiration showed that the mutation(s) for resistance to pyraclostrobin also reduced the sensitivity of mutant strains to other QoIs as azoxystrobin, fluoxastrobin, trifloxystrobin and picoxystrobin, but not to famoxadone and to the QiIs cyazofamid and antimycin-A. An increased sensitivity of pyraclostrobin-resistant strains to the carboxamide boscalid, an inhibitor of complex II, and to the anilinopyrimidine cyprodinil, a methionine biosynthesis inhibitor, was observed. Moreover, no effect of pyraclostrobin resistance mutation(s) on fungitoxicity of the hydroxyanilide fenhexamid, the phenylpyrrole fludioxonil, the benzimidazole benomyl, and to the phenylpyridinamine fluazinam, which affect other cellular pathways, was observed. Study of fitness parameters in the wild-type and pyraclostrobin-resistant mutants of B. cinerea showed that most mutants had a significant reduction in the sporulation, conidial germination and sclerotia production. Experiments on the stability of the pyraclostrobin-resistant phenotype showed a reduction of resistance, mainly in moderate resistant strains, when the mutants were grown on inhibitor-free medium. However, a rapid recovery of the resistance level was observed after the mutants were returned to a selective medium. Studies on the competitive ability of mutant isolates against the wild-type parent strain, by applications of a mixed conidial population, showed that, in vitro, all mutants were less competitive than the wild-type strain. However, the competitive ability of high resistant mutants was higher than the moderate ones. Pathogenicity tests on cucumber seedlings showed that all mutant strains tested exhibited an infection ability similar with the wild-type parent strain. Preventive applications of the commercial product of F-500 25EC (pyraclostrobin) were effective against lesion development on cotyledons by the wild-type, but ineffective, even at high concentrations, against disease caused by the pyraclostrobin-resistant isolates. Boscalid (F-510 50WG) was found equally effective against the disease caused by the wild-type or pyraclostrobin-resistant mutants. This is the first report indicating the appearance of B. cinerea strains resistant to QoI fungicides by the biochemical mechanism of site modification and the risk for field resistance.

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Section: Discussionmentioning

confidence: 99%

Characterization of Laboratory Mutants of Botrytis cinerea Resistant to QoI Fungicides

et al. 2006

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“…The function of the alternative oxidase as a resistance mechanism against QoI has been described in several phytopathogenic fungi (Ziogas et al, 1997;Yukioka et al, 1997;Joseph-Horne et al, 1999;Tamura et al, 1999;Olaya and Ko¨ller, 1999a) but does not appear to play a significant role in field resistance development due to either insufficient ATP formation needed for host infection (Ziogas et al, 1997) or plant flavones, which are released during infection and interfere with the induction of this pathway (Olaya and Ko¨ller, 1999b).…”

Section: Discussionmentioning

confidence: 99%

Biological and molecular characterization of laboratory mutants of Cercospora beticola resistant to Qo inhibitors

et al. 2006

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The resistance to strobilurin-related fungicides and its molecular basis in laboratory mutant isolates of Cercospora beticola was investigated. After ultraviolet mutagenesis, mutants with high, moderate or low resistance levels to pyraclostrobin were isolated from a wild-type strain of C. beticola. Fungitoxicity tests on the response of resistant isolates on medium containing pyraclostrobin and salicylhydroxamate (SHAM), a specific inhibitor of cyanide-resistant (alternative) respiration, indicated that the biochemical mechanism of alternative oxidase was not responsible for the reduced sensitivity to pyraclostrobin for half of the mutants. Cross-resistance studies with other inhibitors of the cytochrome bc 1 complex of the mitochondrial respiratory chain showed that the mutation(s) for resistance to pyraclostrobin also reduced the sensitivity of mutant strains to other Qo inhibitors such as azoxystrobin and fenamidone, but not to the Qi inhibitor cyazofamid. No effect of pyraclostrobin-resistant mutation(s) on fungitoxicity of the carboxamide boscalid, the triazoles epoxiconazole and flutriafol and to the benzimidazole benomyl, which affect other cellular pathways or other steps of the respiratory chain, was observed. Study of fitness parameters showed that most mutants had a significant reduction in sporulation and pathogenicity compared to the wild-type parental isolate. However, experiments on the stability of the resistant phenotype did not show a significant reduction of the resistance for half of the mutants when grown for at least four generations on pyraclostrobin-free medium. Molecular analysis of cytochrome b cDNA, isolated from the wild-type and the pyraclostrobin-resistant mutant isolates, revealed two novel amino acid replacements at positions involved in Qo resistance in other species. The glycine (GGT) to serine (AGT) replacement at position 143 (G143S) was found in the isolate with the highly resistant phenotype. The second amino acid change was the replacement of phenylalanine (TTC) by valine (GTC) at position 129 (F129V), which was found in a mutant strain with the moderately resistant phenotype. Four additional mutations located in conserved regions of the mitochondrial cytochrome b gene (I154L, N250D, E256G and V261D) were detected in some mutant isolates of C. beticola but their possible role in Qo-resistance needs further investigation. This is the first study reporting C. beticola strains resistant to Qo inhibitor fungicides due to the biochemical mechanism of target-site modification, resulting from amino acid changes in the mitochondrial cytochrome b gene.

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“…Studies with sensitive and a resistant mutant isolate of M graminicola ( Septoria tritici Roberge) showed that an efficient alternative respiratory pathway can be one mechanism of resistance to fungicidal respiratory inhibitors acting at the Q o site of cytochrome bc 1 complex 23. This potential bypass of the target site of strobilurin fungicides has also been described in other plant pathogens such as M grisea ,15, 24, 25 Gaeumannomyces graminis (Sacc) v Arx & J Olivier,26–28 B cinerea 29 and V inaequalis 30. 31 However, in vivo experiments showed that the decreased ATP formation by alternative respiration was inadequate for efficient parasitic growth on the host 23.…”

Section: Introductionmentioning

confidence: 85%

A non‐Mendelian inheritance of resistance to strobilurin fungicides in Ustilago maydis

Ziogas

Markoglou

Tzima

2002

Pest Management Science

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Mutants of Ustilago maydis (DC) Corda with high resistance to azoxystrobin (RF 164 to 4714, based on EC50 values), an inhibitor of mitochondrial electron transport at the cytochrome bc1 complex, were isolated in a mutation frequency of 2.3 x 10(-7) after nitrosoguanidine mutagenesis and selection on media containing 1 microgram ml-1 azoxystrobin in addition to 0.5 mM salicylhydroxamate (SHAM), a specific inhibitor of cyanide-resistant (alternative) respiration. Oxygen uptake in whole cells was strongly inhibited in the wild-type strains by azoxystrobin (1.5 micrograms ml-1) in addition to SHAM (1 mM), but not in the mutant isolates. Genetic analysis with nine such mutant isolates resulted in progeny phenotypes which did not follow Mendelian segregation, but satisfied the criteria of non-Mendelian (cytoplasmic) heredity. In crosses between three mutant isolates with the compatible wild-type strains, the sensitivity was inherited by progeny maternally from the wild-type parent strain (criterion of uniparental inheritance). In crosses between wild-type strains and remaining mutant isolates, a continuous distribution of sensitivity in the progeny was found (criterion of vegetative segregation). The third criterion of cytoplasmic resistance (criterion of intracellular selection) was fulfilled by experiments on the stability of resistance phenotypes. With two exceptions, a reduction of resistance was observed in the mutant strains when they were grown on inhibitor-free medium. Recovery of the high resistance level was observed after they were returned to the selection medium. Cross-resistance studies with other fungicides, which also inhibit electron transport through complex III of respiratory chain, showed that mutations for resistance to azoxystrobin were also responsible for reduced sensitivity to kresoxim-methyl (RF 18 to 1199) and to antimycin-A (RF 20 to 305), which act at the Qo and Qi sites of the cytochrome bc1 complex, respectively. Studies of the fitness of azoxystrobin-resistant isolates showed that these mutations appeared to be pleiotropic, having significant adverse effects on growth in liquid culture and pathogenicity on young corn plants.

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Involvement of the alternative oxidase in cellular energy production in the wheat ‘take all’ fungus, Gaeumannomyces graminis var tritici

Cited by 4 publications

References 0 publications

Characterization of Laboratory Mutants of Botrytis cinerea Resistant to QoI Fungicides

Characterization of Laboratory Mutants of Botrytis cinerea Resistant to QoI Fungicides

Biological and molecular characterization of laboratory mutants of Cercospora beticola resistant to Qo inhibitors

A non‐Mendelian inheritance of resistance to strobilurin fungicides in Ustilago maydis

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