Figure 5

Population modelling of vasa -driven HEGs targeting female-specific genes. (A) and (B) HEG constructs targeting a somatic female gene for invasive vector control, (C) HEG constructs targeting a germline-specific female gene for non-invasive vector control. A) The threshold rate of homologous repair in the germline (h _g ) needed for the HEG to invade a population from low frequency, as a function of the overall rate of cleavage. Invasiveness of such a construct is defined as its ability to spread from rare through a population by virtue of genetic drive. The threshold differs depending upon the rate of homing in the embryo (h _e ) (red vs. blue lines). Conversely, with no maternal deposition, the HEG will invade for any h _g >0. (B) Frequency of the HEG and population mean fitness assuming c = 0.9, h _g = 0.9, and an initial release frequency of 1%. Black line: no maternal deposition (D = 0); red line: maternal deposition in which homing rates in the embryo mirror those in the germline (D = 1; h _e = h _g ); blue line: maternal deposition in which all cut sites are repaired exclusively by non-homologous repair (D = 1; h _e = 0). (C) Number of sterile females produced per released male for the HEG-based non-invasive strategy proposed, compared to classical inundative control strategies. To be able to compare to classical measures constructs are released in homozygote males assuming c = 0.9 and for simplicity the models assume that on average one male mates once in his lifetime. c rate of cleavage); h (rate of homologous repair); D (maternal deposition).