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.

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 appendiculatus, Phakopsora 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.

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. triticifield 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.