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.

Exploring Mechanisms of Resistance to Respiratory Inhibitors in Field Strains of Botrytis cinerea , the Causal Agent of Gray Mold

“…In many rusts and in some Alternaria and Agrocybe spp. (55), together with Pyrenophora teres (63), an intron was found after codon 143 that prevented the selection of G143A in cytb, owing to a defect in pre-mRNA splicing leading to the creation of an intron encoding a maturase, as described in yeast (14,51). However, other mutations conferring lower levels of resistance may be selected in these fungi, such as F129L in P. teres (30).…”

Deleterious Effect of the Q o Inhibitor Compound Resistance-Conferring Mutation G143A in the Intron-Containing Cytochrome b Gene and Mechanisms for Bypassing It

“…Interestingly, in those species, the resistance mutation G143A has not been detected so far. In contrast, species where G143A has been reported do not contain intron bi2 (13,24), for instance, Blumeria graminis, Mycosphaerella fijiensis, M. graminicola, Venturia inaequalis, Plasmopara viticola, Alternaria alternata, etc. Botrytis cinerea is particularly interesting, since the same species presents two types of cytochrome b gene; some field isolates contain intron bi2, while others do not.…”

Race Diversity of Pyrenophora tritici-repentis in South Dakota and Response of Predominant Wheat Cultivars to Tan Spot

“…TS alone can cause 5% to 29% yield reduction in South Dakota depending on the inoculum level and cultivar susceptibility under suitable environment for disease development [5]. Excessive use of fungicide could make the pathogen fungicide resistant, reduce its utility and ultimately impact crop productivity [20,21]. In this scenario, development of TS resistant cultivars seems to be the best approach for disease management, especially for a marginally profitable crop like wheat.…”