Table 1.
Embryonic hatching rate from different maternal genetic backgrounds
Maternal genotypeEmbryonic hatching rateMaternal 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 
Maternal genotypeEmbryonic hatching rateMaternal 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.

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