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Genetic control of resistance to fenpropimorph in Ustilago maydis

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dc.contributor.author Markoglou, AN en
dc.contributor.author Ziogas, BN en
dc.date.accessioned 2014-06-06T06:43:57Z
dc.date.available 2014-06-06T06:43:57Z
dc.date.issued 1999 en
dc.identifier.issn 00320862 en
dc.identifier.uri http://dx.doi.org/10.1046/j.1365-3059.1999.00374.x en
dc.identifier.uri http://62.217.125.90/xmlui/handle/123456789/1576
dc.subject Ergosterol biosynthesis inhibitors en
dc.subject Fenpropimorph en
dc.subject Fungicide resistance en
dc.subject Morpholines en
dc.subject Ustilago maydis en
dc.subject.other allele en
dc.subject.other disease control en
dc.subject.other disease resistance en
dc.subject.other fenpropimorph en
dc.subject.other gene locus en
dc.subject.other genetic analysis en
dc.subject.other genetic cross en
dc.subject.other ultraviolet irradiation en
dc.subject.other Ustilago maydis en
dc.title Genetic control of resistance to fenpropimorph in Ustilago maydis en
heal.type journalArticle en
heal.identifier.primary 10.1046/j.1365-3059.1999.00374.x en
heal.publicationDate 1999 en
heal.abstract Fenpropimorph-resistant mutants of Ustilago maydis were obtained at high frequency (30 x 10-6) after UV-irradiation followed by selection on media containing fenpropimorph (50 μg mL-1). Genetic analysis of 30 such mutants resulted in the identification of two unlinked chromosomal loci, the U/fpm-1 locus with two allelic genes (U/fpm-1A and U/fpm-1B) and the U/fpm-2 locus. The mutant genes U/fpm-1A and U/fpm-2 are responsible for high resistance levels (Rf: 75-100 or 257-286 based on MICs or ED(50s), respectively), while the U/fpm-1B mutation gives only a small reduction (approximately 7-10-fold) in fenpropimorph sensitivity. Cross-resistance studies with other SBIs showed that the major gene (U/fpm-1A and U/fpm-2) mutants were cross-resistant to the related compound fenpropidin (Rf: 15-20 or 53-66 based on MICs or ED(50s) values, respectively) and to tridemorph (Rf: 5 or 7.1-9.5 based on MICs or ED(50s) values, respectively), but not to the inhibitors of steps of ergosterol biosynthesis preceding the Δ14-reductase. The minor gene (U/fpm-1B) mutants also had low-level resistance (approximately 5-fold) to tridemorph and to fenpropidin, but in contrast with the major gene mutants they were 2-10 times more sensitive to the triazoles studied (triadimefon, triadimenol, propiconazole and flusilazole) and to the pyridine, pyrifenox. Studies of the fitness of U. maydis mutants showed that in major gene mutants, resistance was not associated with changes in growth rate in liquid culture or pathogenicity on young maize plants. The minor gene mutation reduced significantly the growth rate in liquid culture and the pathogenicity, either in homozygous or heterozygous condition in dikaryotic mycelium. en
heal.journalName Plant Pathology en
dc.identifier.issue 4 en
dc.identifier.volume 48 en
dc.identifier.doi 10.1046/j.1365-3059.1999.00374.x en
dc.identifier.spage 521 en
dc.identifier.epage 530 en


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