CRISPR-Cas9 nuclease-based gene drives rely on inducing chromosomal breaks in the germline that arerepaired in ways that lead to a biased inheritance of the drive. Gene drives designed to impair femalefertility can suppress populations of the mosquito vector of malaria. However, strong unintended fitnesscosts, due to ectopic nuclease expression, and high levels of resistant mutations, limited the potential ofthe first generation of gene drives to spread.Here we show that changes to regulatory sequences in the drive element, designed to contain nucleaseexpression to the germline, confer improved fecundity over previous versions and generate drasticallylower rates of target site resistance. We employed a genetic screen to show that this effect is explainedby reduced rates of end-joining repair of DNA breaks at the target site caused by deposited nuclease inthe embryo.Highlighting the impact of deposited Cas9, many of the mutations arising from this source of nucleaseactivity in the embryo are heritable, thereby having the potential to generate resistant target sites thatreduce the penetrance of the gene drive.Finally, in cage invasion experiments these gene drives show improved invasion dynamics compared tofirst generation drives, resulting in greater than 90% suppression of the reproductive output and a delayin the emergence of target site resistance, even at a resistance-prone target sequence. We shed light onthe dynamics of generation and selection of resistant alleles in a population by tracking, longitudinally,the frequency of resistant alleles in the face of an invading gene drive. Our results illustrate importantconsiderations for future gene drive design and should expedite the development of gene drives robustto resistance.