Insect Control: Biological and Synthetic Agents - Index of

116 A3: Addendum
neonicotinoids in some parts of the world (Elbert
et al., 2008). A laboratory-selected nAChR subunit
Nla1 point mutation (Y151S) observed is most likely
responsible for conferring target-site resistance to
neonicotinoid insecticides in the brown planthopper
N. lugens (Liu et al., 2007). The Y151S mutation has
a significantly reduced effect on neonicotinoid agonist
activity when the subunit Nla1 is coassembled with
Nla2 than when expressed as the sole a-subunit in a
heteromeric nAChR (Liu et al., 2009). A mutation at
this site (Y151M) when introduced into Nla1 and
coexpressed with rat b2 inXenopus oocytes also
showed lower agonist activity (Zhang et al., 2008).
In this context, the possible role of the subunit Nlb1in
neonicotinoid sensitivity was investigated by A-to-I
RNA editing as well (Yao et al., 2009).
One area of major concern over the last decade is
resistance development in B. tabaci (Nauen and
Denholm, 2005). Owing to the obvious advantage
of B. tabaci Q-biotypes in neonicotinoid use environments,
resistance started to spread all over the
world and is now no longer restricted to intense
European cropping systems such as in southern
Spain. Cross-resistance studies with both acetamiprid
and thiamethoxam revealed that the strain
that had been laboratory selected with thiamethoxam
for 12 generations exhibited almost no
cross-resistance to acetamiprid (original strain collected
in the Ayalon Valley late in the cotton-growing
season 2002), whereas the acetamiprid-selected
strain exhibited high cross-resistance of >500-fold
to thiamethoxam (Horowitz et al., 2004). A possible
explanation for the lack of cross-resistance to
acetamiprid in thiamethoxam-selected whiteflies is
selection for different resistant traits (Horowitz
et al., 2004). Resistance in thiamethoxam-selected
whiteflies might be associated with an activation
mechanism, as it has been shown that thiamethoxam
is most probably a pro-drug easily converted to
clothianidin (Jeschke and Nauen, 2007), whereas in
acetamiprid-selected whiteflies the activated compound
itself (clothianidin) is the primary target for
detoxification and results in broad cross-resistance
to all neonicotinoids (Horowitz et al., 2004).
One interesting finding is that resistance to imidacloprid
is age specific in both B- and Q-type strains of
B. tabaci (Nauen et al., 2008). The authors showed
that in contrast to adults exhibiting high levels of
resistance to imidacloprid, young nymphs are still
susceptible. The highest observed resistance ratio
at LD50 expressed in prepupal nymphs was 13,
compared with atleast 580 in their adult counterparts
(Nauen et al., 2008). This has considerable
implications for resistance management strategies,
since targeted nymphs are still well controlled and
selection pressure is released from adults. Neonicotinoid
resistance in B. tabaci is most likely mediated
by CYP6CM1(vQ), a cytochrome P450 monooxygenase
described to be highly over-expressed in female
adults (Karunker et al., 2008), and shown to
hydroxylate imidacloprid at the 5-position of the
imidazolidine ring system when heterologously
expressed in Escherichia coli (Karunker et al.,
2009). Another whitefly species reported to have
developed resistance to neonicotinoids is the greenhouse
whitefly, Trialeurodes vaporariorum (Gorman
et al., 2007; Karatolos et al., 2009). Similar to
B. tabaci, this species also shows cross-resistance
to pymetrozine (Karatolos et al., 2009).
Furthermore, field populations of brown planthoppers,
N. lugens and Sogatella furciera Horváth, resistant
to neonicotinoids have been described in
East and South-East Asia (Gorman et al., 2008;
Matsumura et al., 2008). Mechanistic studies showed
a clear correlation between resistance ratios to
imidacloprid and the extent of O-deethylation of
ethoxycoumarin, indicating that resistance is likely
conferred by monooxygenases similar to that observed
in whiteflies (Puinean et al., in press). Finally,
target-site resistance due to mutations in nAChR
subunits has been suggested to occur in the Colorado
potato beetle L. decemlineata (Tan et al., 2008).
More information on general aspects of insecticide
resistance can be found on the website of the
Insecticide Resistance Action Committee (IRAC,
www.irac-online.org; McCaffery and Nauen, 2006).
The increasing success of neonicotinoids as an
insecticide class also relies on a high degree of versatile
application methods (foliar, seed, or soil treatment),
not seen to the same extent in other chemical
classes (Elbert et al., 2008). New formulations have
been developed for neonicotinoid insecticides
(examples from Bayer CropScience) to optimize
their bioavailability through improved rain fastness,
better retention, and spreading of the spray deposit
on the leaf surface, combined with higher leaf penetration
through the cuticle and translocation within
the plant (Baur et al., 2007; Elbert et al., 2008). The
new formulation technology O-TEQ Õ (oil dispersion,
OD) for foliar application was developed for
imidacloprid (Confidor Õ ) and thiacloprid (Calypso
Õ ) (Baur et al., 2007). The O-TEQ Õ formulations
facilitate leaf penetration, particularly under suboptimal
conditions for foliar uptake.
Combined formulations of neonicotinoids with
pyrethroids such as Confidor S Õ (imidacloprid and
cyfluthrin for control of tobacco pests in South
America), Muralla Õ (imidacloprid and deltamethrin
for vegetable and rice in Central America and
Chile), or Connect Õ (imidacloprid and b-cyfluthrin