Browsing by Subject "Quinone-outside-inhibitor"

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    In vivo und molekularbiologische Untersuchungen zur Sensitivität von Phakopsora pachyrhizi gegenüber Demethylierungs-Inhibitoren und Qo-Inhibitoren
    (2013) Schmitz, Helena Katharina; Vögele, Ralf
    Soybeans are one of the most important crops worldwide. Since 1980, soybean production attained increasing distinction in Brazil. Following the leading producer USA, Brazil counted as the second biggest soybean producer in 2010. A number of threats are involed reducing soybean yield, rating the Asian Soybean Rust, Phakopsora pachyhrizi, as one of the worst pathogens since its invasion in 2001. Until this date the American Soybean Rust, Phakopsora meibomiae, was known in Brazil only, which is of minor importance. Not only did P. pachyrhizi reduce soybean yield in Asia, but also in Brazil considerable additional costs were caused by yield reduction and disease management. Control is mainly based on fungicide treatment, demethylation inhibitors (DMI) and quinone outside inhibitors (QoI) being the most important and effective classes used. Both fungicide groups are frequently applied in combinations to ensure prolonged effects. While efficiency of QoIs remained unchanged, protection by DMIs was significantly narrowed. The primary objective of the recent study was to survey the sensitivity of P. pachyrhizi isolates towards fungicides and to analyse the genetical background of a conceivable adaption. Indeed, an adaption towards DMIs could be observed, while efficiency of QoIs was stable. Due to the P. pachyrhizi genetical structure of the cytochrome b (cyt b) gene, which corresponds to the QoI fungicide target protein, resistance towards QoIs based on the most important mechanism known from other pathogens is rather unlikely. The major resistance mechanism of phytopathogenic fungi against QoIs is an alteration of the cyt b-sequence, in particular point mutations F129L, G137R and G143A, whereas G143A results in highest resistance factors. An intron after codon 143 of the cyt b-gene prevents the development of G143A-mutation. In contrast, genetical analyses of the cyp51-gene, which corresponds to the target protein of DMI fungicides, revealed that adaption is based on different resistance mechanisms which have an additive or synergistic impact. In P. pachyrhizi, point mutations within the cyp51-gene and a modified expression of cyp51 were involved. An altered expression of cyp51 was due to a selective expression of a mutated cyp51-allele and due to up-regulation of cyp51. Six point mutations (F120L, Y131H, Y131F, K142R, I145F and I475T) which appeared in defined combinations, except for one mutation which was found as a single character, correspond to a reduced sensitivity. Additionaly, in some of the isolates cyp51 was up-regulated three- to thenfold compared to the reference strain, leading to decreased efficiency of DMIs. Indications were found, assuming that the copy number of the cyp51-gene in P. pachyrhizi is responsible for the observed alterations in the expression. Other resistance mechanisms than described in the recent study (such as expression of efflux transporters) may additionally play a role now or in future. Resistance towards DMIs evolved by P. pachyrhizi was caused by nesting mechanisms which appeared in quite a short time period due to enormous selection pressure by extensive DMI-use in large areas and the clonal, dicaryotic live cycle with short generation times. Thus, applications of fungicides with different modes of actions are recommended for management of P. pachyrhizi to prevent further resistance development and -distribution.