In Australia, the cotton bollworm, Helicoverpa armigera, has a long history of resistance to

conventional insecticides, Transgenic cotton (expressing Bt toxin Cry1Ac) has been grown

for H. armigera control since 1996.

This project demonstrated that the strain of H. armigera, which came from from the survivors

of Dr Ho Dang’s resistance monitoring programme, are resistant to Cry1Ac toxin (275 fold).

Some 70% of resistant H. armigera were able to survive on Cry1Ac transgenic cotton

(Ingard), a small but significant proportion (5%) also survived on Bollgard II cotton. The

resistance is inherited as a non sex-linked semi-domminant trait. Resistance was associated

with elevated esterase iso-enzyme levels, which were inherited with resistance. Studies of

esterase binding to Cry 1Ac by conventional enzymatic techniques and ground-breaking

surface plasmon resonance real-time bimolecular analysis techniques showed that resistant

strain esterase could bind to Cry1Ac pro-toxin and activated toxin. Studies with live, first

instar larvae, showed that Cry1Ac resistant larvae, fed on Cy1Ac cotton or Cry1Ac treated

artificial diet, had lower esterase activity than non-Cry1Ac fed larvae, thus giving direct

mechanism for the selection of this esterase based resistance mechanism on transgenic cotton.

Cross-resistance studies in the Cry 1Ac resistant strain, showed that Cry 1Ac resistance was

linked to spinosad resistance. Spinosad resistance in H. armigera is also due to esterase

sequestration and thus both Cry 1Ac and spinosad have a common resistance mechanism in

H. armigera. Both Cry 1Ac and spinosad esterase mediated resistances were suppressed by

the insecticide synergist piperonyl butoxide.

Confirmation of Cry1Ac resistance in a strain of H. armigera derived from survivors of a

field Cry1Ac resistance monitoring programme in Australia and findings of an esterase

mediated resistance mechanism that can sequester Cry1Ac, are important to the future of Bt

crops. Of further concern, is the semi-domminant status of the resistance mechanism, which

will make H. armigera resistance management on Bollgard II cotton more difficult. Survival

on transgenic cotton, further emphasises the field significance of resistance to Cry1Ac.

Cry1Ac resistance will place additional selection pressure on the Cry2Ab toxin component of

Bollgard II cotton. Given that H. armigera is a cosmopolitan pest of cotton and other crops,

the finding of an esterase-mediated resistance mechanism may pose a considerable threat to

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the future efficacy of Bt transgenic crops, world-wide. The ability, however, of PBO to

“cross over” from synergising conventional insecticides to synergism of transgenic cotton

against resistant pests represents a considerable breakthrough in the battle to effectively

manage transgenic crops and to retain their efficacy against resistant insects