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are 34 to 51 times the maximal levels reported in Vip3A cotton
plant tissues without any effect on growth.
Early work suggests that the resistance is probably recessive,
which means that insects must carry two copies of the resistance
gene to be able to survive toxin and heterozygotes (RS) are
killed by the toxin. This is particularly fortunate because when
resistance is recessive, field-scale resistance evolves much less
rapidly than when dominant.
Another factor that may affect how fast resistance frequencies
increase within a population is the presence of fitness costs. For
instance, Vip3A resistant insects may have a great advantage on
cotton that expresses Vip3A, but on non-Bt crops they may grow
more slowly or have fewer offspring than susceptible insects.
Early work suggests that, in the laboratory, H. punctigera may
suffer a fitness cost to carrying a resistance gene, but H. armigera
are less affected. If fitness costs are present, a brake may be
applied to increases in resistance.
Will Bollgard III be effective
If Bollgard III expresses Cry1Ac, Cry2Ab and Vip3A toxins
optimally, any Vip3A resistant Helicoverpa that feeds on it should
be killed by one of the Cry toxins.
Unfortunately, protein levels of Cry1Ac have been variable in
the Bt-cotton varieties released to date (Ingard and Bollgard II),
especially later in the season, and this will almost certainly also
be the case in Bollgard III. Research conducted from 2001-03
showed that the ability of Vip3A plants to control susceptible
larvae declined as the season progressed but not as markedly as
for Cry1Ac-expressing plants (Ingard).
Also, especially during flowering, occasional fields of Bollgard
II support larvae that are susceptible to Cry toxins and can survive
to pupation. Presumably during these episodes the expression of
both Cry toxin(s) declines to below toxic levels. Cry2Ab expression
is more stable throughout the season than Cry1Ac expression so
there are probably times where only Cry2Ab is effective which
could select for moths that carry Cry2Ab resistance genes.
This means there is enormous value in protecting the
susceptibility of Helicoverpa species to Cry2Ab until Bollgard
III becomes available. If Cry2Ab is ineffective when Bollgard III
becomes available the Vip3A toxin may be exposed to selection in
a similar fashion to what we assume currently occurs for Cry2Ab
in Bollgard II.
A current CRDC-funded project, which involves collaboration
with Monsanto, is examining the detailed expression profile of
Vip3A in Bollgard III plants. Closer to the commercial release of
Bollgard III, this information will be used with detailed findings
on the characteristics of Vip3A resistance, and the frequencies
of resistance to Cry1Ac, Cry2Ab and Vip3A, to develop a robust
RMP for Bollgard III.
So, although Bollgard III should be very effective against
Helicoverpa species, we don’t yet know the finer details on the
risk of resistance developing to this toxin.
Because the industry began screening populations for Vip3A
resistance before the release of Bollgard III, a firm baseline
frequency will be established prior to any selection occurring
which will allow any increases in resistance to be detected.
1
CSIRO
2
CRDC
The authors greatly appreciate the support of cotton growers who permit
access to crops to collect eggs used in our research. We also thank numerous
technicians, and the Crop Consultants of Australia for collecting eggs for the
work. Expert technical assistance was provided by our colleagues, Janine
Gascoyne, Joel Armstrong and Tracey Parker.
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December 2012–January 2013 The Australian Cottongrower — 19