No Gug³⁵ mutant males expressing Gug^{dsRNA.1.Scer\UAS} under the control of Scer\GAL4^dpp.blk1 develop melanotic masses in their heads.

Gug³⁵ clones in the eye disc do not induce the formation of additional photoreceptor cells. However, in 20.1% of cases, ommatidia in Gug³⁵ clones have 5, instead of 4, cone cells.

Gug³⁵ clones in the wing show autonomous development of extra vein tissue.

Homozygous clones at the tip of the antenna result in aristae which are fatter and shorter than normal.

Homozygous clones at the tip of the leg result in reduced claws which resemble bristles.

Homozygous clones result in almost complete loss of the ocellar triangle region, with a single ocellus often being the only structure remaining.

Homozygous clones result in defects in the wing margin; in the proximal anterior region, the large wide central bristles that normally develop in the triple row in this region are thinner and longer than normal and in the posterior region, the bristles develop a socket and are longer than normal, indicating a partial transformation to the anterior fate.

Homozygous clones in the eye can non-autonomously affect the polarity of wild-types cells at the polar border of the clone; wild-type ommatidia at the polar border of dorsal clones adopt a ventral appearance, while wild-type and mosaic ommatidia at the equatorial border of the clone have normal polarity. Planar polarity is also disrupted within the clone. Ommatidia within the clones often appear to have lost one or more outer photoreceptors and in many cases they have more than one inner photoreceptor with smaller rhabdomeres.

Symmetrical ommatidia are often seen in the eyes of Gug¹¹/Gug³⁵ flies, mostly of the R4/R4 achiral subtype.

Homozygous clones in the eye are similar in size to their twin-spots.

Homozygous clones in the eye disc appear strikingly smooth when they are located anterior to the morphogenetic furrow. This smoothness is lost after progression of the furrow.

Homozygous clones in the wing produce blisters where the dorsal and ventral surfaces of the wing fail to fuse.

Homozygous clones in the thorax disrupt thorax closure, resulting in a cleft in the dorsal thorax.

Homozygous embryos (lacking zygotic Gug function) show defects in head morphogenesis (this is the only mutant phenotype in these embryos). Embryos lacking maternal Gug function (derived from females with homozygous germline clones fertilised with wild-type sperm) have severe segmentation defects. Embryos lacking both maternal and zygotic Gug function lack ventral pattern elements and have holes in the ventral cuticle. Homozygous clones induced at different stages of development are found in all parts of the leg with a frequency similar to Gug⁺ clones showing that Gug⁺ function is not required for cell viability. The clones are always restricted to the anterior or posterior compartment and do not change the overall segmental identity of the legs. Homozygous clones in the dorsal or lateral parts of the leg give rise to essentially wild-type patterns, although there is a slight cell autonomous increase in bristle density in mutant clones compared to wild type. Mutant clones in the ventral part of the leg delete specific pattern elements and replace them with pattern elements resembling those normally formed in more lateral distal regions of the leg; the large ventral bristles of the posterior compartment of the femur of the first leg, the apical bristle at the distal tip of the anterior tibia, the spur bristles at the tip of each tarsal segment and the transverse row and sex comb bristles of the first leg are not formed in mutant clones. Ventral clones in the anterior or posterior compartments result in fusion of the femur to the tibia. Large mutant clones in the coxa, trochanter or proximal femur lead to fusion of these segments. Clones in these proximal parts of the leg generally have bracts (typical of bristles that occur more distally in wild-type legs). Clones in dorsal regions do not affect proximal identity, however, large clones that occupy both dorsal and ventral domains replace all patterns with more distal identities and cause a reversal of bristle polarity. These large clones have a non-autonomous effect on the polarity of more distally located, ventral bristles. Small clones in the ventral part of the leg lead to outgrowths forming a partial new axis (a complete new leg is never formed). The bristles in these outgrowths have a distal identity (they have bracts). The outgrowths consist of both mutant and Gug⁺ tissue.

Gug³⁵/Gug[+] is a suppressor of abnormal locomotor behavior | adult stage phenotype of mir-8^Δ2/Df(2R)mir-8^Δ3

Gug³⁵/Gug[+] is a suppressor | partially of partially lethal phenotype of mir-8^Δ2/Df(2R)mir-8^Δ3

Gug³⁵, gro^Eal13/gro[+] has visible | dominant phenotype

Gug³⁵/Gug[+], sbb⁶ has visible | dominant phenotype

Gug³⁵/Gug[+], sbb^Eal17 has visible | dominant phenotype

Gug³⁵, gro^E48/gro[+] has visible | dominant phenotype

Df(2R)en^E/+, Gug³⁵ has visible | dominant phenotype

Gug³⁵, ft^G-rv/ft¹ has lethal | dominant phenotype

Gug³⁵, ft⁸/ft¹ has lethal | dominant phenotype

Gug³⁵, ft^chance/ft¹ has lethal | dominant phenotype

Gug³⁵/Gug[+] is an enhancer of wing vein | ectopic phenotype of rl^Sem

Gug³⁵/Gug[+] is an enhancer of interommatidial bristle phenotype of rho^hs.sev

Gug³⁵/Gug[+] is an enhancer of ommatidium phenotype of rho^hs.sev

Gug³⁵ is an enhancer of phenotype of al^unspecified

Gug³⁵/Gug[+] is a suppressor | partially of leg phenotype of mir-8^Δ2/Df(2R)mir-8^Δ3

Gug³⁵/Gug[+] is a suppressor of interommatidial bristle phenotype of aos^GMR.PC

Gug³⁵/Gug[+] is a suppressor of ommatidium phenotype of aos^GMR.PC

Gug³⁵, gro^Eal13/gro[+] has interocellar bristle phenotype

Gug³⁵/Gug[+], sbb⁶ has interocellar bristle phenotype

Gug³⁵/Gug[+], sbb^Eal17 has interocellar bristle phenotype

Gug³⁵, gro^E48/gro[+] has interocellar bristle phenotype

Df(2R)en^E/+, Gug³⁵ has interocellar bristle phenotype

Gug³⁵, ft^G-rv/ft¹ has eye phenotype