Joel Mackay and Ron Hill – with collaborators Emily Remnant, Chris McErlean and Nathan Lo
Most insecticides are non-selective, but 99% of insect species are ‘good guys’, meaning that there is a lot of collateral ecological damage that comes from the application of such molecules – particularly at an industrial scale.
Our goal is to develop insecticides that target a chosen pest species selectively, while not impacting relevant beneficial insect species.
How are we planning to do that? By focusing on the fact that the biology of all insects (and more broadly, Arthropods – spiders, mites, ticks) is controlled by the steroid hormone ecdysone. Ecdysone activity controls almost every aspect of Arthropod development, physiology and behaviour. The hormone acts by binding to the transcription factor ecdysone receptor (EcR) – which is a member of the same family of proteins as the perhaps more familiar transcription factors estrogen/androgen receptors, glucocorticoid receptor and retinoic acid receptor.
We are hoping to exploit amino acid sequence differences between the EcR protein in different insect orders and to therefore design molecules that can inhibit a pest EcR but not the EcR of a beneficial insect.
There are many possible pests that we could pursue but our first test case is to consider the honeybee and its pests – the Varroa mite and the small hive beetle. Can we make molecules that strike these pests but not the nearby honeybee…? We shall see!