The dot-like small eye phenotype characteristic for flies expressing egr^Scer\UAS.cMa under the control of Scer\GAL4^GMR.PFa is partially suppressed by combination with Rac1^J10, together with Rac2^Δ and Mtl^Δ, all in heterozygous state.

Rac1^J11/Rac1^J10, Rac2^Δ, Mtl^Δ triple mutant larvae exhibit strong ECM detachment and epithelial enclosure of dendrites in class IV dendritic arborizing neurons.

After single cell wounding (by laser ablation), Rac triple mutant embryos (Rac1^J10, Rac2^Δ, Mtl^Δ) show severe disruption of actin cortical flow, affecting both actin ring and actin halo formation, resulting in wound overexpansion and an aberrant oval (rather than rounded) wound shape.

Heterozygosity for Rac1^J10 Rac2^Δ Mtl^Δ suppresses the axonal defects found in N^l1N-ts1 mutants.

Heterozygosity for a Rac1^J10 Rac2^Δ Mtl^Δ triple mutant chromosome does not alter arm⁸ mutant patterning nor its rate of hatching.

One copy of each of Rac1^J10, Rac2^Δ and Mtl^Δ fails to suppress the lethality seen when pbl^{ΔN-term.Scer\UAS.T:Ivir\HA1} is expressed under the control of Scer\GAL4^GMR.PU.

One copy of each of Rac1^J10, Rac2^Δ and Mtl^Δ strongly suppresses the rough eye phenotype seen when pbl^{DH-PH.Scer\UAS.T:Ivir\HA1} is expressed under the control of Scer\GAL4^GMR.PU.

Stage 8 embryos lacking zygotic and maternal expression of Rac1^J10, Rac2^Δ and Mtl^Δ display mesoderm migration defects.

The Scer\GAL4^elav-C155/DAAM^{C.Scer\UAS.P\T} gain-of-function phenotype (i.e the appearance of thicker commissures and nerve roots) is not affected by Rac1 gene dose (i.e. a Rac1^J11/Rac1^J10 background).

Heterozygosity for Rac1^J10 Rac2^Δ Mtl^Δ suppresses the RhoGAP18B¹ ethanol-resistance phenotype.

Rac1^J10/+ suppresses the decrease in dorsal cluster neuron axon extension of hep¹ mutants.

Rac1^J10 Rac2^Δ Mtl^Δ triple mutant germ line clone embryos exhibit failure in germband retraction, head involution and dorsal closure. Not all of these phenotypes are fully penetrant; embryos with the least severe phenotype show only failure in dorsal closure. The epithelial cells of these embryos lack both actin cables and actin protrusions at the leading edges. The leading edge of zygotic Rac1^J10 Rac2^Δ Mtl^Δ triple mutants is somewhat disordered. Some of the cells in the mutant edge assemble the actin cable and actin projections, while other cells fail to do so. Cells without protrusions halt the "zipper" that closes the dorsal hole. However, the mutant exhibits a compensatory mechanism in which new zippering fronts emerge after the actin deficient stretches to complete closure.

Mosaic border follicle cell clusters, which contain some wild-type cells and some cells with the genotype Rac1^J10 Rac2^Δ Mtl^Δ/Rac1^J10 Rac2^Δ Mtl⁺ show impaired migration.

Homozygous Rac1^J10 Rac2^Δ embryos derived from homozygous Rac1^J10 Rac2^Δ female germline clones show mild defects in macrophage migration as macrophages do not disperse into the ventral posterior trunk region by stage 14 or 15. By late embryogenesis, macrophages have dispersed throughout the entire ventral trunk in these embryos. Sibling embryos that are derived from homozygous Rac1^J10 Rac2^Δ female germline clones but are zygotically heterozygous for Rac1^J10 Rac2^Δ (having received a paternal wild-type copy of Rac1 and Rac2) show a normal distribution of macrophages.

Homozygous Rac1^J10 Rac2^Δ Mtl^Δ embryos derived from homozygous Rac1^J10 Rac2^Δ Mtl^Δ female germline clones show the same macrophage migration defects as homozygous Rac1^J10 Rac2^Δ embryos derived from homozygous Rac1^J10 Rac2^Δ female germline clones.

Rac1^J10 Rac2^Δ Mtl^Δ triple mutant embryos (lacking both maternal and zygotic function of the Rac1, Rac2 and Mtl genes) fail to complete dorsal closure. There is little or no actin accumulation at the leading epidermal edge and both lamellipodia and filopodia are lacking. The underlying amnioserosa cells appear normal. Little or no myoblast fusion occurs in these embryos. Severe axon growth defects are seen; in the CNS, Fas2-positive axons rarely extend from one segment into the next and very few sensory axons from the PNS reach the CNS. Specification of neuronal and glial cell fate and dendritic growth and morphology appears relatively normal. Rac1^J10 Mtl^Δ double mutant embryos (lacking both maternal and zygotic function of the Rac1 and Mtl genes) show dorsal closure defects. Myoblast fusion appears complete in these embryos. Rac1^J10 Rac2^Δ double mutant embryos (lacking both maternal and zygotic function of the Rac1 and Rac2 genes) show dorsal closure defects. Little or no myoblast fusion occurs in these embryos. Rac1^J10 enhances the frequency of midline guidance defects in Mtl^Δ mutant embryos to 75%. Axon stalling is occasionally seen in the double mutant embryos. Less than 2% of Rac1^J10 Rac2^Δ mutant embryos show midline guidance defects (Fas2-positive longitudinal axons crossing the midline). Mosaic flies in which the eye is doubly mutant for Rac1^J10 and Rac2^Δ show mild defects in the projection pattern of photoreceptor cell axons. Mosaic flies in which the eye is doubly mutant for Mtl^Δ and Rac1^J10 show defects in the projection pattern of photoreceptor cell axons, showing a medulla bypass phenotype. Mosaic flies in which the eye is triply mutant for Mtl^Δ, Rac1^J10 and Rac2^Δ show severe defects in the projection pattern of photoreceptor cell axons, showing a medulla bypass phenotype. The projection defects in the triple mutant eyes can be rescued by Rac1^GMR.PNe or Mtl^GMR.PN.

Rac1^J10 Rac2^Δ Mtl^Δ triple mutant embryos exhibit no significant retardation of wound closure.