Twospotted spider mite, Tetranychus urticae (Fig.1), is one of the most destructive mite pests of greenhouse-grown horticultural crops. Twospotted spider mite populations are difficult to manage due to the following characteristics: 1) they feed on a wide-range of plants; 2) females have a high reproductive capacity; 3) they have a short life cycle (egg to adult); 4) multiple generations can occur simultaneously; and 5) rapid population growth. Therefore, miticides (acaricides) are routinely applied to suppress or mitigate twospotted spider mite populations from reaching damaging levels, which will reduce substantial damage to plants. However, the twospotted spider mite can rapidly develop resistance to many pesticides (insecticides and miticides).
A number of commercially available miticides are known as mitochondria complex electron transport inhibitors or METI. The mitochondrion (plural: mitochondria) is a membrane-bound organ that is a major site where chemicals in food are converted into energy in the form of adenosine triphosphate (ATP) that is utilized in metabolic processes in cells. In some cases, cytochrome proteins may be involved, which facilitates electron transport and allows for oxidation-reduction reactions (reactions that involve gaining or losing electrons) to occur.
Miticides that are classified as METI include: acequinocyl (Shuttle), bifenazate (Floramite), cyflumetofen (Sultan), fenazaquin (Magus), fenpyroximate (Akari), and pyridaben (Sanmite). In general, the METI are active on all life stages of the twospotted spider mite including the egg, larva, nymph, and adult. However, studies have shown that METI miticides are more active on the nymph and adult life stages of the twospotted spider mite. Furthermore, METI miticides are only active as contact miticides; they do not have translaminar activity (material penetrates leaf tissues and forms a reservoir of active ingredient within the leaf; thus providing activity even after residues on the leaf dry) as do some miticides such as abamectin (Avid), chlorfenapyr (Pylon), etoxazole (TetraSan/Beethoven), spiromesifen (Savate) and spirotetramat (Kontos).
The basic mode of action of the METI is through the reduction of energy production in the mitochondrion by disrupting or inhibiting the production of ATP, which leads to rapid paralysis and death as a consequence of cellular energy starvation. The mode of action of the METI involves activity on three different complexes (I, II, and III) (Fig. 2). Below are the three complexes and how the miticides act on these complexes along with the associated active ingredients (in parentheses):
- Complex I: inhibit nicotinamide adenine dinucleotide hydride (NADH) dehydrogenase associated with electron transport or act on NADH by binding to coenzyme site Q (CoQ) reductase (fenazaquin, fenpyroximate and pyridaben)
- Complex II: inhibit functioning of complex by affecting the active site after being metabolized to AB-1 (cyflumetofen)
- Complex III: bind to the quinone oxidizing (Qo) center in the cytochrome bc1 subunit (acequinocyl and bifenazate)
Tolfenpyrad (Hachi-Hachi) is also a METI acting on Complex I but is not a miticide, with registration for use against aphids, mealybugs, thrips and whiteflies. Table 1 presents the pesticides (insecticides and miticides) designated as mitochondria complex electron transport inhibitors (METI) along with the complex target site in the mitochondrion, and the Insecticide Resistance Action Committee (IRAC) designation.
The METI miticides are effective against most life stages (i.e. egg, larva, nymph, and adult) of the twospotted spider mite; however, it is important to avoid using METI miticides in succession (back-to-back) in spray programs to prevent twospotted spider mite populations from developing resistance to this mode of action.