The dot-like small eye phenotype characteristic for flies expressing egr^Scer\UAS.cMa under the control of Scer\GAL4^GMR.PFa cannot be suppressed by combination with Rac2^Δ in heterozygous state.

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.

Pupal retina constituting almost entirely of somatic clones (induced specifically in the eye) triple homozygous for Rac2^Δ,Rac1^J11,Mtl^Δ do not show any extra cone cells or primary pigment cells, only extra inter-ommatidial cells are observed.

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.

The mushroom bodies of Rac1^J11 Rac2^Δ Mtl^Δ triple heterozygotes display short α/β axonal lobes compared with those of controls. The peduncle and ellipsoid body form normally.

The mushroom body axons of flies that are heterozygous for Rac1^J11, Rac2^Δ tsr^N96A sick^Δ and Mtl^Δ fail to extend to form peduncles and lobe structures (the 'posterior arrest' phenotype).

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.

The presence of Rac2^Δ/+, Rac1^J11/+ and Mtl^Δ/+ mutations fails to suppress the reduction of differentiation seen in eye-antennal disc clones expressing both RhoGEF2^RE.Scer\UAS and Ras85D^{G12V.Scer\UAS} under the control of Scer\GAL4^tub.PU, and also fails to suppress the developmental delay shown by larvae containing these clones.

Only small amounts of muscle fibers form in Rac1^J11, Rac2^Δ mutant embryos - these myofibers round up upon muscle contraction, indicating detachment.

Co-expression of Ced-12^Scer\UAS.cGa and mbc^Scer\UAS.cBa via Scer\GAL4^Mef2.PR results in prevalent myoblast fusion, muscle attachment, and tendon cell identity phenotypes in embryos. The muscle attachment and tendon cell phenotypes are largely rescued in a Rac1^J11/+, Rac2^Δ/+ background.

Zir^BG00267/+ ; Rac2^Δ/+ double heterozygous larvae have a reduced rate of encapsulation (42%) of eggs of the avirulent wasp strain L. boulardi G486 compared to the rate seen in either single heterozygote.

Myoblast fusion is defective in Rac1^J11 Rac2^Δ double mutant embryos, although some fusion does occur. Binucleate muscle precursors that have undergone a single fusion event between a founder cell and a fusion competent myoblast are seen in the mutant embryos as follows: DA1 (64.2% of segments), DO1 (68.3% of segments), LO1 (26.3% of segments), VT1 (66.7%) of segments.

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.

Expression of psidin^Scer\UAS.cKa under the control of Scer\GAL4^slbo.2.6 in a Rac1^J11 Rac2^Δ double heterozygous background has little or no effect on border cell migration.

No rhabdomeric defect is seen at the base of the rhabdomere at eclosion in flies in which the eyes are triply mutant for Rac1^J11 Rac2^Δ Mtl^Δ, although there is an axon guidance defect in the optic lobe.

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.

The eye phenotype seen when vav^{Δ1-207.Scer\UAS.T:Ivir\HA1} is expressed under the control of Scer\GAL4^GMR.PU is suppressed in a homozygous Rac2^Δ background. The phenotype is not suppressed in a Rac2^Δ/+ background.

Larval hemocytes prepared from flies simultaneously heterozygous for drpr^Δ5, Rac1^J11 and Rac2^Δ show a significant reduction in the level of phagocytosis of S. aureus.

Heterozygosity for Rac2^Δ has no effect on the phenotype in the alpha lobes of the mushroom bodies that is seen in PsGEF^Δ21 animals.

prtp^Δ1/+ ; Rac1^J11 Rac2^Δ/+ triple heterozygotes show a reduced level of phagocytosis in embryonic hemocytes (neither prtp^Δ1/+ single heterozygotes nor Rac1^J11 Rac2^Δ/+ double heterozygotes show a reduction in phagocytosis compared to wild type).

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 supresses 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 rough eye phenotype resulting from Scer\GAL4^GMR.PU-mediated expression of Ced-12^Scer\UAS.cGa and mbc^Scer\UAS.cBa is suppressed by heterozygosity for Rac1^J11, Rac2^Δ.

A Rac1^J11 Rac2^Δ Mtl^Δ heterozygous background enhances the patterning defects found in Scer\GAL4^GMR.PF>cindr^{dsRNA.PC.PD.Scer\UAS} mutants. The mean interommatidial precursor cell number and the number of cone and/or 1[o] cell errors is increased in these double mutants.

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 a Rac1^J11, Rac2^Δ background or a Rac1^J10, Rac2^Δ, Mtl^Δ background.

A Rac1^J11/+; Rac2^Δ/+ background enhances both the zygotic DAAM^Ex68 and DAAM^Ex68; Rac1^J11/+ CNS phenotypes.

A Rac1^J11; Rac2^Δ, Mtl[Δ] heterozygous background enhances the zygotic DAAM^Ex68, DAAM^Ex68; Rac1^J11/+ and DAAM^Ex68; Rac1^J11/+; Rac2^Δ/+CNS phenotypes.

Rac1^J11, Rac2^Δ, Mtl^Δ triple mutant clones in the eye result in a low frequency (approximately 5%) of planar polarity defects (such as achiral or misrotated ommatidia). Cdc42⁵, Rac1^J11, Rac2^Δ, Mtl^Δ quadruple mutant clones in the eye result in a higher frequency of (14.2%) of planar polarity defects.

The salivary gland defects seen in Rac1^J11 embryos are enhanced in Rac1^J11 Rac2^Δ mutants; more cells remain at the ventral surface of the embryo and the gland fails to migrate posteriorly. In addition, the lumen of the salivary gland is disrupted, with breaks in the lumen being seen during posterior migration of the gland, and cyst-like lumena being seen in the mature gland.

shi² Rac1^J11 Rac2^Δ Mtl^Δ heterozygous embryos form normal salivary glands at the permissive temperature of 25[o]C. However, at the restrictive temperature of 30[o]C, posterior migration of the salivary gland is disrupted.

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

The Rac2^Δ mutation fails to modify the cv-c^M62 phenotype in the Malpighian tubules. Dorsal closure defects occur in 82% of Rac1^J11, Rac2^Δ double mutant embryos. If these mutants also carry the cv-c^M62 mutation , 37% of these embryos are rescued. In cv-c^M62, Rac1^J11, Rac2^Δ triple mutants, the posterior spiracle phenotype is enhanced compared to cv-c^M62 mutants. Posterior spiracle phenotypes are seen in Rac1^J11, Rac2^Δ embryos, but with low penetrance.

In Rac1^J11; Rac2^Δ double homozygous embryos, rearrangement of tubule cells to produce elongated, 2 cell wide tubules is partially disrupted and tubule migration is defective. The anterior tubules follow an erratic path, doubling back on themselves to form loops and knots.

Both Rac1^J11, Rac2^Δ/Rac2^Δ mutants and Rac2^Δ, Rac1^J11/Rac1^J11 mutants show a reduction of 5-HT arborization in the larval brain.

Developmental dispersal of hemocytes is abnormal in embryos triply mutant for Rac1^J11, Rac2^Δ and Mtl^Δ.

One hour after laser-induced wounding, approximately half the number of hemocytes are recruited to the wound in embryos triply mutant for Rac1^J11, Rac2^Δ and Mtl^Δ compared to wild type embryos. Hemocytes that are recruited in the triple mutant embryos have significantly reduced lamellar protrusions.

Contacts between the invaginated mesoderm and the ectoderm fail to be established properly in embryos derived from females with reduced Rac2 and Rac1 function. Contacts between the invaginated mesoderm and the ectoderm fail to be established properly in embryos derived from females with reduced Mtl, Rac2 and Rac1 function.

Germ line clones of the Rac1^J11 Rac2^Δ Mtl^Δ triple mutant fail to produce embryos. Zygotic Rac1^J11 Rac2^Δ Mtl^Δ triple mutants, that have wild-type maternal contribution of Rac1, survive beyond early dorsal closure, but still show 100% embryonic lethality. These embryos achieve dorsal closure, but show puckering along the dorsal side. The dorsal hole becomes a long slit-like shape as it closes in the triple mutants, while the hole has an oval shape in wild-type embryos. Although amnioserosa cells are significantly larger in the mutant than in wild type, these cells are able to contract at a similar rate to wild type. The leading edge of zygotic Rac1^J11 Rac2^Δ Mtl^Δ triple mutants is disorganized and, unlike in wild-type embryos, is not taut. Many of the triple mutant leading edge cells are polygonal in shape, instead of being dorsally-ventrally elongated, like in wild type. Some of the cells in the mutant edge assemble the actin cable and actin projections, while other cells fail to do so. Leaky expression of hep^CA.Scer\UAS, with no GAL4 driver, partially rescues the lethality and dorsal puckering phenotype of Rac1^J11 Rac2^Δ Mtl^Δ triple 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.

Rac1^J10 Rac2^Δ Mtl^Δ triple mutant embryos (lacking both maternal and zygotic function of the Rac1, Rac2 and Mtl genes) are able to almost completely dominantly suppress the sti^{dsRNA.Sym.Scer\UAS} (under the regulation of Scer\GAL4^ey.PB) phenotype, reverting the eye to wild-type size and appearance. Rac1^J10 Rac2^Δ Mtl^Δ triple mutant embryos (lacking both maternal and zygotic function of the Rac1, Rac2 and Mtl genes) are able to dominantly suppress the RacGAP50C^{dsRNA.Scer\UAS} (under the regulation of Scer\GAL4^ey.PB) eye phenotype.

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.

Rac1^J11, Rac2^Δ or mutant embryos exhibit arrested ganglionic branches (GBs), and GBs turning prematurely away from the midline. robo⁴ partially suppresses the ganglionic branch phenotype seen in Rac1^J11, Rac2^Δ embryos.

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.

Double mutant clones of Rac1^J11 and Rac2^Δ do not affect F-actin enrichment in rhabdomeres.

In a subset of the epidermis of stage 15 Rac1^J11, Rac2^Δ double homozygous embryos the distinction between apical and basolateral domains is compromised. At stage 16 the columnar epithelial cells are shorter than wild-type and parts of the epidermis become multilayered. Rac1^J11, Rac2^Δ double homozygous embryos exhibit a variety of tracheal defects: The mildest phenotype is a misrouting of the dorsal branches toward the anteroposterior direction, whereas more severely effected embryos also exhibit truncations of the dorsal trunk.

The combination of heterozygous sli² and Rac2^Δ leads to longitudinal axon ectopic midline crossing defects. An average of 1.4 defects are seen per animal, and an average of 13% of segments have defects.

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 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. Rac2^Δ Mtl^Δ double mutant embryos (lacking both maternal and zygotic function of the Rac2 and Mtl genes) successfully complete dorsal closure. A few isolated myoblasts fail to fuse in these embryos. Rac1^J11 Rac2^Δ Mtl^Δ triple mutant clones in the wing and eye do not show planar cell polarity defects. Rac2^Δ enhances the frequency of midline guidance defects in Mtl^Δ mutant embryos to 42%. 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 Rac1^J11 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 Rac2^Δ show mild defects in the projection pattern of photoreceptor cell axons. 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. Mosaic flies in which the eye is triply mutant for Mtl^Δ, Rac1^J11 and Rac2^Δ show severe defects in the projection pattern of photoreceptor cell axons, showing a medulla bypass phenotype. Specification of photoreceptor cell fate appears to be normal.

55% of Rac1^J11 Rac2^Δ double mutant neuroblast clones show defective guidance. 55% of Rac1^J11 Rac2^Δ Mtl^Δ single-cell γ neuron clones in the mushroom body show axon-stalling defects, mostly at the peduncle. There is a significant reduction in total dendritic length and number of dendritic segments per neuron compared to wild type. Mushroom body axon growth defects in single-cell Rac1^J11 Rac2^Δ Mtl^Δ γ neuron clones are largely rescued by expression of Rac1^{Scer\UAS.T:Hsap\MYC} or Rac1^{Y40C.Scer\UAS.T:Hsap\MYC} under the control of Scer\GAL4^OK107. Mushroom body axon growth defects in single-cell Rac1^J11 Rac2^Δ Mtl^Δ γ neuron clones are not rescued by expression of Rac1^{F37A.Scer\UAS.T:Hsap\MYC} under the control of Scer\GAL4^OK107. 81% of axons in Rac1^J11 Rac2^Δ mushroom body clones show mutant phenotypes, predominantly guidance (55%) and branching (24%) defects. Expression of Rac1^{Scer\UAS.T:Hsap\MYC} under the control of Scer\GAL4^OK107 markedly rescues these defects. Expression of Rac1^{Y40C.Scer\UAS.T:Hsap\MYC} under the control of Scer\GAL4^OK107 does not reduce the total percentage of axonal defects in Rac1^J11 Rac2^Δ mushroom body clones, but results in a marked shift in the distribution of defects, with most showing branching (45%) rather than guidance (31%) defects. Analysis of Rac1^J11 Rac2^Δ mushroom body clones indicates cell non-autonomous effects in axon guidance and branching caused by defective "Rac" activity.

The phenotype caused by expression of msn^EP549 under the control of Scer\GAL4^GMR.PF is not modified by the addition of the triple mutant combination Rac1^J11 Rac2^Δ Mtl^Δ.

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