Figure 6

SDKR can, under certain conditions, achieve significant and localised population suppression. Results shown are for strategies based on dominant (a–c) or recessive (d–f) female to male sex conversion and dominant (g–i) or recessive (j–l) female-specific lethality. Heat maps display the equilibrium genetic load imposed on a target (left column; blue) and a non-target population (centre column; orange). Black contour lines are shown for genetic loads of 80%, 90%, 95% and 99%. Here, the equilibrium state is assessed 1000 generations after the release of transgenic individuals. The right column shows specific examples for parameter combinations indicated by coloured dots in the left and centre columns (i.e. combinations of homing rate \(\Phi =0.6\) or 0.9 and female to male sex conversion (\(\delta =0.5\) or 0.9) or female-specific lethality (\(\gamma =0.5\) or 0.9)). Solid lines represent transgene allele frequencies in a target population and dashed lines are the equivalent for a non-target population. In all cases, simulations consider a relative fitness of \(\varepsilon =0.95\) per construct (applied multiplicatively) and fully penetrant lethal effects (i.e. \(L=1\)). In each case we consider the release of individuals homozygous for both transgenic constructs and fitness costs that are applied multiplicatively. Migration is considered to be unidrectional at a rate of 2% per generation. It is also worth noting that fitness costs associated with transgenic constructs can produce a small genetic load even where sex conversion and/or female-specific lethality are absent. Supplementary Figures S1 and S2 show equivalent results for fitness costs of 15% and 10% per construct, respectively and demonstrate the importance of fitness costs in determining the ability of such systems to produce confined population suppression.