Table 1. Embryonic hatching rate from different maternal genetic backgrounds.
| Maternal genotype | Embryonic hatching rate | Maternal genotype |
|---|---|---|
| Control (w/+; nos-Gal4VP16/+) | 92.4% | n = 463 |
| KhcmutA/KhcmutA | 48.8% | n = 172 |
| nos>Klc-RNAi + Btz-RNAi | 19.1% | n = 591 |
| KhcmutA/KhcmutA; nos>Klc-RNAi + btz-RNAi | 0% | n = 388 |
| nos>Khc-RNAi | 0% | n = 458 |
| nos>Khc-RNAi + Unc104-KTail | 0.8% | n = 358 |
| stau[D3]/stau[ry9] | 0% | n = 205 |
| stau[D3]/stau[ry9]; nos>Staufen-SunTag | 82.2% | n = 118 |
Single inhibition of either streaming (by KhcmutA) or directed transport along microtubules (by Klc and btz double RNAi) maternally led to a reduced embryonic hatching rate. The inhibition of directed transport had a stronger effect on embryo hatching rates than the inhibition of streaming. Simultaneous inhibition of streaming and directed transport caused complete failure of embryogenesis comparable with knockdown of KHC (Khc-RNAi). Partial rescue of streaming by the expression of a chimeric motor (Unc104-KTail) in Khc knockdown background did not rescue the embryonic lethality. Lack of Staufen (stau[D3]/stau[ry9]) caused embryonic lethality, while ectopic expression of Staufen-SunTag maternally significantly suppressed the embryonic lethality resulting from the absence of endogenous Staufen.