The toxin and antidote puzzle: new ways to control insect pest populations through manipulating inheritance

Abstract

Insects carry out essential ecological functions, such as pollination, but also cause extensive damage to agricultural crops, and transmit human diseases such as malaria and dengue fever. Advances in insect transgenesis are making it increasingly feasible to engineer genes conferring desirable phenotypes, and gene drive systems are required to spread these genes into wild populations. Medea provides one solution, being able to spread into a population from very low initial frequencies through the action of a maternally-expressed toxin linked to a zygotically-expressed antidote. Several other toxin-antidote combinations are imaginable that distort the offspring ratio in favor of a desired transgene, or drive the population towards an all-male crash. We explore two such systems--Semele, which is capable of spreading a desired transgene into an isolated population in a confined manner; and Merea, which is capable of inducing a local population crash when located on the Z chromosome of a Lepidopteron pest.

Figure 1

Novel toxin-antidote gene drive systems for controlling insect pest populations. (A) Medea, named after the character from Greek mythology, distorts the offspring ratio in its favor through the action of a maternally-expressed toxin gene and a zygotically-expressed antidote gene. (B) This enables Medea to spread into a population from low initial frequencies. (C) Semele, named after the mortal female from Greek mythology, distorts the offspring ratio in its favor through the action of a semen-based toxin and a female-specific antidote. (D) In the absence of a fitness cost, Semele spreads into a population for release frequencies exceeding ∼36%. (E) Merea distorts the offspring ratio in its favor through the action of a maternal toxin and a recessive zygotic antidote. (F) If located on the Z chromosome of a species for which females are the heterogametic sex, Merea is capable of inducing an all-male population crash for release frequencies exceeding ∼50%.