The dot-like small eye phenotype characteristic for flies expressing egrScer\UAS.cMa under the control of Scer\GAL4GMR.PFa is partially suppressed by combination with Rac1J10, together with Rac2Δ and MtlΔ, all in heterozygous state.
Pupal retina constituting almost entirely of somatic clones (induced specifically in the eye) triple homozygous for Rac2Δ,Rac1J11,MtlΔ do not show any extra cone cells or primary pigment cells, only extra inter-ommatidial cells are observed.
After single cell wounding (by laser ablation), Rac triple mutant embryos (Rac1J10, Rac2Δ, MtlΔ) 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 Rac2Δ/+, Rac1J11/+ and MtlΔ/+ mutations fails to suppress the reduction of differentiation seen in eye-antennal disc clones expressing both RhoGEF2RE.Scer\UAS and Ras85DG12V.Scer\UAS under the control of Scer\GAL4tub.PU, and also fails to suppress the developmental delay shown by larvae containing these clones.
A mild, though not significant enhancement of the ommatidium-phenotype resulting from the co-expression of Arf51FGD13822 with Dcr-2Scer\UAS.cDa under the control of Scer\GAL4GMR.PF is observed in a Rac1J11, Rac2Δ, MtlΔ heterozygous background.
No rhabdomeric defect is seen at the base of the rhabdomere at eclosion in flies in which the eyes are triply mutant for Rac1J11 Rac2Δ MtlΔ, although there is an axon guidance defect in the optic lobe.
A Rac1J11 Rac2Δ MtlΔ heterozygous background enhances the patterning defects found in Scer\GAL4GMR.PF>cindrdsRNA.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.
Rac1J11, Rac2Δ, MtlΔ triple mutant clones in the eye result in a low frequency (approximately 5%) of planar polarity defects (such as achiral or misrotated ommatidia). Cdc425, Rac1J11, Rac2Δ, MtlΔ quadruple mutant clones in the eye result in a higher frequency of (14.2%) of planar polarity defects.
shi2 Rac1J11 Rac2Δ MtlΔ 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.
One hour after laser-induced wounding, approximately half the number of hemocytes are recruited to the wound in embryos triply mutant for Rac1J11, Rac2Δ and MtlΔ compared to wild type embryos. Hemocytes that are recruited in the triple mutant embryos have significantly reduced lamellar protrusions.
Germ line clones of the Rac1J11 Rac2Δ MtlΔ triple mutant fail to produce embryos. Zygotic Rac1J11 Rac2Δ MtlΔ 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 Rac1J11 Rac2Δ MtlΔ 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 hepCA.Scer\UAS, with no GAL4 driver, partially rescues the lethality and dorsal puckering phenotype of Rac1J11 Rac2Δ MtlΔ triple mutants. Rac1J10 Rac2Δ MtlΔ 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 Rac1J10 Rac2Δ MtlΔ 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.
Rac1J10 Rac2Δ MtlΔ triple mutant embryos (lacking both maternal and zygotic function of the Rac1, Rac2 and Mtl genes) are able to almost completely dominantly suppress the stidsRNA.Sym.Scer\UAS (under the regulation of Scer\GAL4ey.PB) phenotype, reverting the eye to wild-type size and appearance. Rac1J10 Rac2Δ MtlΔ triple mutant embryos (lacking both maternal and zygotic function of the Rac1, Rac2 and Mtl genes) are able to dominantly suppress the RacGAP50CdsRNA.Scer\UAS (under the regulation of Scer\GAL4ey.PB) eye phenotype.
Homozygous Rac1J10 Rac2Δ MtlΔ embryos derived from homozygous Rac1J10 Rac2Δ MtlΔ female germline clones show the same macrophage migration defects as homozygous Rac1J10 Rac2Δ embryos derived from homozygous Rac1J10 Rac2Δ female germline clones.
The combination of heterozygous sli2 and MtlΔ 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.
Rac1J10 Rac2Δ MtlΔ 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. Rac1J10 MtlΔ 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. Rac2Δ MtlΔ 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. Rac1J11 Rac2Δ MtlΔ triple mutant clones in the wing and eye do not show planar cell polarity defects. Rac1J10 enhances the frequency of midline guidance defects in MtlΔ mutant embryos to 75%. Axon stalling is occasionally seen in the double mutant embryos. Rac2Δ enhances the frequency of midline guidance defects in MtlΔ mutant embryos to 42%. Mosaic flies in which the eye is doubly mutant for MtlΔ and Rac2Δ show mild defects in the projection pattern of photoreceptor cell axons. Mosaic flies in which the eye is doubly mutant for MtlΔ and Rac1J10 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 MtlΔ, Rac1J10 and Rac2Δ 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 Rac1GMR.PNe or MtlGMR.PN. Mosaic flies in which the eye is triply mutant for MtlΔ, Rac1J11 and Rac2Δ 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 Rac1J11 Rac2Δ MtlΔ 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 Rac1J11 Rac2Δ MtlΔ γ neuron clones are largely rescued by expression of Rac1Scer\UAS.T:Hsap\MYC or Rac1Y40C.Scer\UAS.T:Hsap\MYC under the control of Scer\GAL4OK107. Mushroom body axon growth defects in single-cell Rac1J11 Rac2Δ MtlΔ γ neuron clones are not rescued by expression of Rac1F37A.Scer\UAS.T:Hsap\MYC under the control of Scer\GAL4OK107.