Mutations in the mitochondrial cytochrome b of Tetranychus urticae Koch (Acari: Tetranychidae) confer cross‐resistance between bifenazate and acequinocyl

Abstract

Although there is no absolute cross-resistance between bifenazate, acequinocyl and fluacrypyrim, some bifenazate resistance mutations confer cross-resistance to acequinocyl. In the light of resistance development and management, high prudence is called for when alternating bifenazate and acequinocyl in the same crop. Maternally inherited cross-resistance between bifenazate and acequinocyl reinforces the likelihood of bifenazate acting as a mitochondrial complex III inhibitor at the Q(o) site.

Sublethal effects of two common acaricides on the consumption of Tetranychus urticae (Prostigmata: Tetranychidae) by Phytoseius plumifer (Mesostigmata: Phytoseiidae)

“…Bifenazate belongs to the group of hydrazine derivatives (Van Leeuwen et al 2010), and is being used worldwide for control of spider mites on several crop systems (Dekeyser 2005;Van Leeuwen et al, 2015). Recent studies reported that the resistance of T. urticae to bifenazate is tightly linked to the mutations in the mitochondrial cytochrome b (cytb) and the Q 0 site of cytb complex III of the electron transport chain (Van Leeuwen et al 2008;Van Nieuwenhuyse et al 2009). Reciprocal crosses between the susceptible and resistant mites showed that the resistance was only inherited maternally (non-Mendelian), supporting a hypothesis called mitochondrial control (Van Leeuwen et al 2006).…”

Acaricides - Biological Profiles, Effects and Uses in Modern Crop Protection

“…5) is highly effective against immatures and adults of spider mites, with rapid knockdown effect (Ochiai et al, 2007). Although it was first considered to be a neurotoxin, more recent experimental results indicate complex III as target site (van Nieuwenhuyse et al, 2009). Bifenazate is a pro-acaricide which is bioactivated via hydrolysis of ester bonds, so the organophosphorous compounds, as inhibitors of esterase hydrolitic activity, can antagonize the toxicity of this acaricide .…”

“…Although the monogenic and dominant resistance has been expected due to intense selection pressure to which the populations under the open field or greenhouse conditions are exposed (Roush & McKenzie, 1987), some major exceptions occur, such as the monogenic-recessive resistance to dicofol (Rizzieri et al, 1988), propargite (Keena & Granett, 1990), pyridaben (Goka, 1998) and etoxazole (Uesugi et al, 2002), and poligenic resistance to cyhexatin (Mizutani et al, 1988). Lately, several studies dealing with molecular basis of the target site resistance to pyrethroids Kwon et al, 2010b), organophosphates (Khajehali et al, 2010;Kwon et al, 2010a) and bifenazate (van Leeuwen et al, 2008, van Nieuwenhuyse et al, 2009) have been published. Especially interesting discovery is that the bifenazate resistance in T. urticae is inherited only maternally, which is the first occurrence of non-Mendelian inheritance since the beginning of genetic studies on pesticide resistance in arthropods (van Leeuwen et al, 2008, van Nieuwenhuyse et al, 2009.…”

“…Lately, several studies dealing with molecular basis of the target site resistance to pyrethroids Kwon et al, 2010b), organophosphates (Khajehali et al, 2010;Kwon et al, 2010a) and bifenazate (van Leeuwen et al, 2008, van Nieuwenhuyse et al, 2009) have been published. Especially interesting discovery is that the bifenazate resistance in T. urticae is inherited only maternally, which is the first occurrence of non-Mendelian inheritance since the beginning of genetic studies on pesticide resistance in arthropods (van Leeuwen et al, 2008, van Nieuwenhuyse et al, 2009. Biological, biochemical and genetic characterization of resistance is one of the essential elements in defining the strategy for management of acaricide resistance in phytophagous mites.…”

Trichopolyn VI: a new peptaibol insecticidal compound discovered using a recombinant <i>Saccharomyces cerevisiae</i> screening system

“…Insecticidal tolerance caused by genetic alterations is normally responsible for mechanisms that either reduce the effect of an insecticide on its target site or lead to a decrease in insecticide kinetics, such as absorption, distribution, metabolism and excretion (Herron et al, 2003;Kaufman et al, 2001;Khalighi et al, 2014;Kim et al, 2004;Van Leeuwen et al, 2010;Van Nieuwenhuyse et al, 2009). Therefore, it is necessary to develop new insecticides, particularly those that have a novel mode of action, to help overcome the global increase in insecticide-resistant agricultural pests.…”