How Its Works?
Homozygous adult males of OX513A strain of Aedes aegypti which do not bite are released to mate with wild females and pass on the self-limiting gene to produce heterozygous progeny that die in the absence of specific antidote (tetracycline) (at the late larval stage in Ae. aegypti) before they attain adulthood and hence eventual suppression of the population. With repeated releases of sufficient numbers of these self-limiting males, there is a reduction in the wild population to below the level needed to transmit disease according to models of disease transmission.
Oxitec genetic control works by inserting a gene into the target organism, which prevents the insect from surviving to adulthood. The gene produces a protein called tTAV (tetracycline repressible activator variant), which can control the activity of other genes by acting as a switch. It's a gene variant that has been optimised to only work in insect cells. In the engineered insects, when the tTAV gene is expressed, the non-toxic protein ties up the cell's machinery so its other genes aren't expressed and the insect dies. The proteins produced are non-toxic in the insects, so if any animals eat them it would be the same as eating a wild insect – they will be digested in just the same way that all other insects are digested.
To continue producing the insects there's an antidote, tetracycline given to the insects in the rearing medium that binds to the tTAV protein disabling the tTAV proteins functions. So in the presence of the antidote, the Oxitec insects are able to survive and reproduce in the rearing facility, but when the males are released into the wild, their offspring of fathered by released male mosquitoes can't survive in the absence antidote in the natural environment, so they die before reaching adulthood.