title: Cytochrome b gene sequence and structure of Pyrenophora teres and P. tritici-repentis and implications for QoI resistance.
abstract: Resistance to QoI fungicides in Pyrenophora teres (Dreschsler) and P. tritici-repentis (Died.) Dreschsler was detected in 2003 in France and in Sweden and Denmark respectively. Molecular analysis revealed the presence of the F129L mutation in resistant isolates of both pathogens. In 2004, the frequency of the F129L mutation in populations of both pathogens further increased. The G143A mutation was also detected in a few isolates of P. tritici-repentis from Denmark and Germany. In 2005, the F129L mutation in P. teres increased in frequency and geographical distribution in France and the UK but remained below 2% in Germany, Switzerland, Belgium and Ireland. In P. tritici-repentis, both mutations were found in a significant proportion of the isolates from Sweden, Denmark and Germany. The G143A mutation conferred a significantly higher level of resistance (higher EC50 values) to Qo inhibitors (QoIs) than did the F129L mutation. In greenhouse trials, resistant isolates with G143A were not well controlled on plants sprayed with recommended field rates, whereas satisfactory control of isolates with F129L was achieved. For the F129L mutation, three different single nucleotide polymorphisms (SNPs), TTA, TTG and CTC, can code for L (leucine) in P. teres, whereas only the CTC codon was detected in P. tritici-repentis isolates. In two out of 250 isolates of P. tritici-repentis from 2005, a mutation at position 137 (G137R) was detected at very low frequency. This mutation conferred similar resistance levels to F129L. The structure of the cytochrome b gene of P. tritici-repentis is significantly different from that of P. teres: an intron directly after amino acid position 143 was detected in P. teres which is not present in P. tritici-repentis. This gene structure suggests that resistance based on the G143A mutation may not occur in P. teres because it is lethal. No G143A isolates were found in any P. teres populations. Although different mutations may evolve in P. tritici-repentis, the G143A mutation will have the strongest impact on field performance of QoI fungicides.
authors.affiliation: Syngenta Crop Protection, Research Biology, 4332 Stein, Switzerland. helge.sierotzki@sygenta.com
authors.forename: Helge
authors.initials: H
authors.lastname: Sierotzki
authors.forename: Regula
authors.initials: R
authors.lastname: Frey
authors.forename: Jürg
authors.initials: J
authors.lastname: Wullschleger
authors.forename: Simona
authors.initials: S
authors.lastname: Palermo
authors.forename: Serge
authors.initials: S
authors.lastname: Karlin
authors.forename: Jeremy
authors.initials: J
authors.lastname: Godwin
authors.forename: Ulrich
authors.initials: U
authors.lastname: Gisi
mesh_terms: D000595:Amino Acid Sequence; D000935:Antifungal Agents / Q000494:pharmacology; D001203:Ascomycota / Q000187:drug effects / Q000201:enzymology / Q000235:genetics*; D001665:Binding Sites; D045303:Cytochromes b / Q000737:chemistry / Q000235:genetics*; D025141:Drug Resistance, Fungal / Q000235:genetics*; D014450:Electron Transport Complex III / Q000037:antagonists & inhibitors; D001467:Hordeum / Q000378:metabolism; D008969:Molecular Sequence Data; D020125:Mutation, Missense; D020641:Polymorphism, Single Nucleotide; D016415:Sequence Alignment; D014908:Triticum / Q000378:metabolism
chemical_list: D000935:Antifungal Agents; D045303:Cytochromes b; D014450:Electron Transport Complex III