Compared with wild-type, interommatidial precursor cells (IPCs) co-expressing Arf51F^GD13822 and Dcr-2^Scer\UAS.cDa under the control of Scer\GAL4^GMR.PF exhibit weak cell extensions that seldom extend sufficiently far to reach a target primary pigment cell and are often retracted. When contact is occasionally achieved by the mutant cells, in contrast to wild-type, the IPC-primary pigment cell interface fails to rapidly widen and is commonly lost. Rather than generating one concerted extension, IPCs co-expressing Arf51F^GD13822 and Dcr-2^Scer\UAS.cDa via Scer\GAL4^GMR.PF typically produce multiple small extensions or none at all. Arf51F^GD13822-expression also induces some ectopic apoptosis prior to 20 h after puparium formation (APF). Impaired cell intercalation disrupts the final arrangement of cells in mature Scer\GAL4^GMR.PF>Arf51F^GD13822, Dcr-2^Scer\UAS.cDa eyes: few secondary or tertiary niches are correctly occupied, IPCs frequently cluster into multiple rows, and the IPC lattice is poorly organised, leading to "fusion" of some ommatidia. Minor defects in cone and primary pigment cell organization and orientation are also present at low frequency.

The patterning defects in retinas co-expressing Arf51F^GD13822 and Dcr-2^Scer\UAS.cDa under the control of Scer\GAL4^GMR.PF is enhanced by heterozygosity for Arf51F^ΔKG1.

The patterning defects in retinas co-expressing Arf51F^GD13822 and Dcr-2^Scer\UAS.cDa under the control of Scer\GAL4^GMR.PF is enhanced by heterozygosity for In(1)rst³.

The patterning defects in retinas co-expressing Arf51F^GD13822 and Dcr-2^Scer\UAS.cDa under the control of Scer\GAL4^GMR.PF is enhanced by heterozygosity for hbs⁴⁵⁹.

The eye mis-patterning phenotype resulting from the co-expression of Arf51F^GD13822 with Dcr-2^Scer\UAS.cDa under the control of Scer\GAL4^GMR.PF is significantly enhanced in ArfGAP3^e01250 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 eye mis-patterning phenotype resulting from the co-expression of Arf51F^GD13822 with Dcr-2^Scer\UAS.cDa under the control of Scer\GAL4^GMR.PF is significantly enhanced in Asap1^KG03963 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 eye mis-patterning phenotype resulting from the co-expression of Arf51F^GD13822 with Dcr-2^Scer\UAS.cDa under the control of Scer\GAL4^GMR.PF is significantly enhanced in siz^T1032 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 eye mis-patterning phenotype resulting from the co-expression of Arf51F^GD13822 with Dcr-2^Scer\UAS.cDa under the control of Scer\GAL4^GMR.PF is significantly enhanced in Efa6^KO1 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.

Compared with wild-type, the actin cytoskeleton is less well-organised in retinal cells co-expressing Arf51F^GD13822 with Dcr-2^Scer\UAS.cDa under the control of Scer\GAL4^GMR.PF.

A mild, though not significant enhancement of the ommatidium-phenotype resulting from the co-expression of Arf51F^GD13822 with Dcr-2^Scer\UAS.cDa under the control of Scer\GAL4^GMR.PF is observed in a Rac1^J11, Rac2^Δ, Mtl^Δ heterozygous background.

Heterozygosity for Rho1^72F enhances the patterning defects in the retina of flies co-expressing Arf51F^GD13822 with Dcr-2^Scer\UAS.cDa under the control of Scer\GAL4^GMR.PF.

The ommatidial patterning defects resulting from the co-expression of Arf51F^GD13822 with Dcr-2^Scer\UAS.cDa driven by Scer\GAL4^GMR.PF are mildly enhanced in Df(3R)Exel8194 heterozygotes. However, the genetic interaction does not achieve statistical significance.