Introduction and General Information

The working group is responsible for global fungicide resistance strategies in the Qo inhibitor fungicides (QoI). The Qo inhibitor fungicides all act at the Quinone ‘outer’ (Qo) binding site of the cytochrome bc1 complex.

They are all in the same cross-resistance group and should be managed accordingly.

Code Target site of action Chemical group Common name Comments
11 Complex III;
cytochrome bc1
(ubiquinol oxidase)
at Qo site (cyt b gene)
methoxy-acrylates azoxystrobin
coumoxystrobin
enoxastrobin
flufenoxystrobin
picoxystrobin
pyraoxystrobin
Resistance known in various fungal species. Target site mutations in cyt b gene (G143A, F129L) and additional mechanisms.

Cross resistance shown between all members of the QoI group.

High risk.

See FRAC QoI Guidelines for resistance management.
Methoxy-acetamide mandestrobin
methoxy-carbamates pyraclostrobin
pyrametostrobin
triclopyricarb
oximino-acetates kresoxim-methyl
oximino-acetamides dimoxystrobin
fenaminostrobin
metominostrobin
oxazolidine-dones famoxadone
dihydro-dioxazines fluoxastrobin
imidazolinones fenamidone
benzyl-carbamates pyribencarb

The Qo fungicides inhibit plant pathogens by blocking the pathogens ability to produce energy. They do this by blocking the transfer of electrons at the Quinone "outside" site of the bc1 complex (complex III in the electron transport chain). There are two other fungicidal target sites at complex III, the Quionone "inside" (Qi) site (FRAC group 21) and the Quinone "outside" Stigmatellin binding (QoS) sub site (FRAC group 45). The members of the Qo group (FRAC group 11) are cross-resistant with each other but are not cross-resistant with members of the QiI (FRAC group 21) or QoSI (FRAC group 45).

The QoIs are active against a broad range of  plant pathogens including representatives of all three important genera of plant pathogens, the ascomycetes, basidiomycetes and oomycetes. Most of the members of the class are registered broadly on a large number of crops although a few members are registered for use on a narrower spectrum of crops and diseases. As each member of the group has its particular strengths, label recommendations for specific products should always be followed.

The first members of the QoIs were launched in 1996. Isolates of Blumeria graminis f sp. tritici (Sierotzki et al. 2000) and Plasmopara viticola (Heaney et al. 2000) resistant to QoIs were found a short time later. They were found to have a mutation in the cytochrome b gene that caused the protein to change from Gly to Ala at position 143 (G143A). For a list of plant pathogens where isolates resistant to QoIs were found see Species with QoI Resistance (Status Dec. 2012).

Mutations associated with QoI-resistance

The three amino acid substitutions detected in the cytochrome b gene that govern resistance to Qo inhibitors in plant pathogens are:

  • Change from glycine to alanine at position 143 (G143A)

  • Change from phenylalanine to leucine at position 129 (F129L)

  • Change from glycine to arginine at position 137 (G137R)

All G143A, G137R and F129L are based on single nucleotide polymorphisms in the cytochrome b gene; the selection process is qualitative (single step).

Based on current knowledge, resistance factors (RF= ED50 [resistant strain] / ED50 [sensitive or wild-type strain]) associated with G143A, G137R and F129L are different. RFs attributed to G143A are in most cases greater than 100 and usually greater than several hundreds. Isolates carrying G143A express high (complete) resistance. Isolates with F129L or G137R express moderate (partial) resistance. QoIs applied at manufacturers’ recommended rates are shown to provide effective control of diseases with the F129L or G137R mutation. In contrast, a severe loss in disease control is always seen in populations where G143A predominates and QoIs are used alone.


For more information and a list of references, please see  Mutations Associated with QoI Resistance.

Effect of Intron at G143A on Resistance Development 


In some species the amino acid substitution of the alanine for the glycine at position 143 has not been observed despite significant use of the QoIs against these species in the field. In different Puccinia species as well as Alternaria solani and Pyrenophora teres, an intron (non-coding region of DNA) was observed directly after the triplet GGT that encodes for glycine (Grasso et al. 2006). It is predicted that the nucleotide subsitution resulting in the alanine at position 143 is lethal since this substution will strongly affect the splicing process, leading to a deficient cytochrome b (Grasso et al. 2006). As a consequence, resistance to QoI fungicides based on the G143A mutation is not likely to evolve in species such as rusts (Puccinia spp., Uromyces appendiculatusPhakopsora pachyrhizi, Hemileia vastatrix), P. teres and A. solani. The presence of such an intron has also been reported in Monilinia laxa, Monilinia fructicola (Miessner and Stammler 2010, Luo et al. 2010) and Guignardia bidwellii (Miessner et al. 2011). However, it cannot be excluded that mutations other than G143A conferring reduced sensitivity may arise in upcoming populations selected by the use of QoI fungicides. For A. solani and P. teres the mutations F129L and/or G137R have been reported (Sierotzki et al. 2007) as a mechanism for QoI tolerance. Both mutations are of minor importance, however, because they generally lead to lower resistance factors than the G143A mutation and it has been found that these two mutations have no, or only limited impact on the field efficacy of QoIs (Semar et al. 2007).

For more information and additional references, please see Impact of Intron.

References


Grasso V, Palermo S, Sierotzki H, Garibalid A, Gisi U. Cytochrome b gene structure and consequences for resistance to Qo inhibitor fungicides in plant pathogens. Pest Management Science 2006; 62(6):465-472.

Heaney SP, Hall AA, Davis SA, Olaya G. Resistance to fungicides in the QoI-STAR cross resistance group: current perspectives. In The BCPC Conference: Pests and disease, Volume 2. Proceedings of an international conference held at the Brighton Hilton Metropole Hotel, Brighton, UK, 13-16 November 2000. Brighton, UK: Brighton Crop Protection Council; 2000. pp. 755-762.

Luo CX, Hu M, Luo CX, Hu MJ, Jin X, Bryson PK, Schnabel G. Evidence for the unlikely development of the QoI fungicide resistance-related G143A mutation in the Cyt b gene of Monilinia fructicola.  Pest Management Science 2010; 66:1308–1315.

Miessner S., Mann W, Stammler G. Guignardia bidwellii, the causal agent of black rot on grapevine has a low risk for QoI resistance. Journal of Plant Diseases and Protection 2011; 118(2), 51-53.

Miessner S., and Stammler G. Monilinia laxa, M. fructigena and M. fructicola: Risk estimation of resistance to QoI fungicides and identification of species with cytochrome b gene sequences. J. Plant Dis. Prot. 2010; 117:162-167.

Semar M., Strobel D, Koch A, Klappach K, Stammler G.  Field efficacy of pyraclostrobin against populations of Pyrenophora teres containing the F129L mutation in the cytochrome b gene. J. Plant Dis. Prot. 2007; 114:117-119.

Sierotzki H, Wullschleger J, Gisi U. Point-mutation in cytochrome b gene conferring resistance to strobilurin fungicides in Erysiphe graminis f. sp. tritici field isolates. Pesticide Biochemistry and Physiology 2000; 68:107-112.

Sierotzki H, Frey R.  Cytochrome b gene sequence and structure of Pyrenophora teres and P.tritici-repentis and implications for QoI resistance. Pest Manag. Sci. 2007; 63:225-233.

 

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Contact

Helge Sierotzki
Interim Chair

Syngenta Crop Protection Münchwilen AG 
WST540.1.94 
CH-4332 Stein

Tel : +41 62 866 01 80 
Fax: +41 62 866 07 63

E-Mail: Helge Sierotzki