74bp deletion in exon 8.
Cultured neurons from stage 11 Efa6KO1 embryos show a small but significant increase in axon length, with a significantly higher density of branches, as compared to controls. Growth cones show increased microtubule polymerization, as there is a significant increase in the number of EB1 comets at growth cones and growth cone filopodia. There are significantly more growing microtubules (EB1 comets) in filopodia along the axon shaft, but not in the axon shaft itself, as compared to controls. Axonal microtubules become progressively more disorganized, as compared to controls.
Efa6c00953/Efa6KO1 are more sensitive (lower survival) to ethanol than wild-type controls.
Naive Efa6c00953/Efa6KO1 mutants show preference for ethanol-laced food, unlike the aversion normally observed in wild-type controls. Efa6c00953/Efa6KO1 mutants previously exposed to ethanol show the same preference for ethanol-laced food as wild-type controls.
Efa6KO1/CG31158[+] is an enhancer of ommatidium phenotype of Scer\GAL4GMR.PF, cindrRNAi.PC.PD.UAS
Efa6KO1/CG31158[+] is an enhancer of retina phenotype of Arf6GD13822, Dcr-2UAS.cDa, Scer\GAL4GMR.PF
Efa6KO1/CG31158[+] is an enhancer of ommatidium phenotype of Arf6GD13822, Dcr-2UAS.cDa, Scer\GAL4GMR.PF
Efa6KO1/CG31158[+] is an enhancer of primary pigment cell phenotype of Arf6GD13822, Dcr-2UAS.cDa, Scer\GAL4GMR.PF
Efa6KO1/CG31158[+] is an enhancer of secondary pigment cell phenotype of Arf6GD13822, Dcr-2UAS.cDa, Scer\GAL4GMR.PF
Efa6KO1/CG31158[+] is an enhancer of tertiary pigment cell phenotype of Arf6GD13822, Dcr-2UAS.cDa, Scer\GAL4GMR.PF
Efa6KO1/CG31158[+] is an enhancer of cone cell phenotype of Arf6GD13822, Dcr-2UAS.cDa, Scer\GAL4GMR.PF
Efa6KO1/CG31158[+] is an enhancer of interommatidial precursor cell phenotype of Arf6GD13822, Dcr-2UAS.cDa, Scer\GAL4GMR.PF
The eye mis-patterning phenotype resulting from the co-expression of Arf51FGD13822 with Dcr-2Scer\UAS.cDa under the control of Scer\GAL4GMR.PF is significantly enhanced in Efa6KO1 heterozygotes. The number of correctly patterned secondary and tertiary cell is reduced. The total number of interommatidial precursor cells (IPCs) does not differ markedly from the wild-type number of 12, indicating that the enhancement is due to specifically to increased disorder in IPC patterning. Additionally, errors in the placement of three bristle groups about each ommatidium and errors in primary pigment cell and cone cell patterning and ommatidial rotation are modestly enhanced.
The ommatidial patterning errors resulting from the expression of cindrdsRNA.PC.PD.Scer\UAS via Scer\GAL4GMR.PF are strongly enhanced in Efa6KO1 heterozygotes.