Sep. 30, 2002 FORT COLLINS -- Insecticide resistance is one of the most widespread genetic changes caused by human activity, and scientists are only now beginning to understand these changes that allow global populations of insects to evolve resistance and become unaffected by pesticides. A new study by a team of worldwide researchers, including Colorado State University biology professor Tom Wilson, has made a major scientific breakthrough in understanding the genetics of insecticide resistance.
In a paper to be published in the Sept. 27 edition of the journal Science, Wilson and his colleagues identify the gene responsible for resistance in Drosophila, the common fruit fly. The ability of this fly to develop pesticide resistance is due to a mutation in a single gene known as DDT-R. The team's new research results show that the overactivity of this gene alone is both necessary and sufficient for insecticide resistance.
"It is common for insecticides to work well for several years but then loose their effectiveness, because insects evolve resistance to these poisons," said Wilson. "Because it is difficult to conduct genetic research on most pest insects, the genetics of this evolution has long remained a mystery. However, our current research has identified, for the first time, a gene responsible for insecticide resistance and how it became mutated in a model insect."
To dissect the genetic basis of insecticide resistance, Wilson and his colleagues conducted research on global populations of fruit flies. The genome of this insect was sequenced in 2000, giving the team a powerful tool to conduct research and understand genetic changes associated with insecticide resistance. Using Drosophila as a genetic model, Wilson and his team investigated the insect resistance that has arisen worldwide to dichlorodiphenyltrichloroethane, or DDT. Research into insects' resistance to this pesticide also gives insight to a range of other existing and novel insecticides.
An insect's resistance to pesticides revolves around the DDT-R gene. DDT-R produces a metabolic enzyme known as cytochrome P450, which is the agent responsible for breaking down DDT and other poisons. Normally these metabolic enzymes, found in all living organisms from bacteria to humans, are present in low amounts. However, Wilson and his colleagues found that when insects become resistant to pesticides, there is a dramatic increase in the amount of one of these enzymes due to the overexpression of the DDT-R gene.
This occurs because the DDT-R gene becomes mutated by insertion of another piece of the fly's DNA, known as a transposable genetic element, or jumping gene, into the controlling sequence of the gene. This insertion messes up the normal expression of DDT-R, leading to over-production of its product, the cytochrome P450 metabolic enzyme. The result is that, as soon as an insecticide enters the body of the insect, it is broken down so efficiently that the poisons never reach their target tissue to cause death.
"Insecticide resistance is an amazing process and important to understand," said Wilson. "We are witnessing evolutionary changes in a population in a matter of years, rather than in millions of years. This research is, in part, telling us how living organisms respond to all of the chemicals we put out into the world."
Another important result of the study is that the team found insecticide-resistant populations of fruit flies all over the world, even in areas where the pesticide DDT has not been used for many years. In the United States, Japan, Russia, Europe and elsewhere, the resistant Drosophila all have exactly the same mutation. The implication is that a resistant population of fruit flies arose from a single mutational event and spread worldwide. Furthermore, although fruit flies are not direct targets of insecticides, they are still affected by them.
According to Wilson, "This is both interesting and scary. This research indicates that at least one non-pest insect and likely other creatures are being influenced by the many pesticides being used throughout the world."
Wilson added that the study highlights how human use of pesticides is, in effect, greatly speeding up resistance by natural selection process among insects. He offered an example of how a resistance genetic mutation can spread so quickly: "If a farmer has a field with 17 billion pest insects and uses a new pesticide, 16.9 billion are immediately susceptible and are killed. The resistant ones survive and pass on the resistance gene to the next generation. Now, the resistant group makes up a larger percentage of the whole.
"The farmer sprays later in the growing season and again kills many pests, but primarily susceptible ones. After a few more times using the insecticide, there is an increasingly larger percentage of the population that is resistant."
Other members of the research team include researchers from the United Kingdom, Australia and France. Another American author of the paper is Scott Jeffers, who contributed to the work as an undergraduate student at Colorado State and now is in a doctoral program at Purdue University. Wilson said that this is just one example of the prominence of undergraduate research as part of regular coursework at Colorado State.
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