filopodium & embryonic leading edge cell, with Scer\GAL4en-e16E
The expression of Lmon\actAFP4mito.UAS.EGFP under the control of Scer\GAL4how-24B, Scer\GAL4HCH.Hand or Scer\GAL4GMR31F09 leads the embryonic heart exhibiting holes between contralateral cardioblasts; in the Scer\GAL4how-24B-driven expression setting, the holes primarily occur between Svp-expressing CBs. In the Scer\GAL4GMR31F09-driven expression setting, some cardioblasts do not make proper shape changes necessary for attachment. In the Scer\GAL4[GMR31F09]-driven expression setting, migrating cardioblasts show fewer and shorter filopodia.
Late third instar wing disc clones expressing Zzzz\actAFP4mito.Scer\UAS.T:Avic\GFP-EGFP under the control of Scer\GAL4sd-SG29.1 exhibit increased boundary cell proliferation, compromising the dorsal-ventral affinity boundary.
89% of eggs derived from females expressing Zzzz\actAFP4mito.Scer\UAS.T:Avic\GFP-EGFP under the control of Scer\GAL4mat.αTub67C.T:Hsim\VP16 show a "dumpless" phenotype.
Egg chambers expressing Zzzz\actAFP4mito.Scer\UAS.T:Avic\GFP-EGFP under the control of Scer\GAL4mat.αTub67C.T:Hsim\VP16 do not show obvious alterations in cortical actin levels or organisation prior to dumping, but there is a striking defect in the cytoplasmic filaments (the bundled cytoplasmic actin filaments extending from the cortex to nuclei); many fewer cytoplasmic filaments form in the mutant egg chambers, those that do form do so later than normal and are usually restricted to nurse cells nearest the oocyte. The formation of ring canal-associated actin filaments is also reduced and delayed in the mutant egg chambers. Most of the mutant egg chambers have nurse cell nuclei that protrude into ring canals, which often results in nurse cells in terminal egg chambers retaining cytoplasm.
No defects in ring canal formation or growth are seen in egg chambers expressing Zzzz\actAFP4mito.Scer\UAS.T:Avic\GFP-EGFP under the control of Scer\GAL4mat.αTub67C.T:Hsim\VP16.
Approximately 50% of border cell clusters expressing Zzzz\actAFP4mito.Scer\UAS.T:Avic\GFP-EGFP under the control of Scer\GAL4slbo.2.6 fail to reach the oocyte by early stage 10 (compared to a failure of less than 10% in wild-type egg chambers), even though the long cellular extensions required to initiate migration appear normal. The migration speed is significantly slower in the mutant border cells compared to controls.
Leading edge cells expressing Zzzz\actAFP4mito.Scer\UAS.T:Avic\GFP-EGFP under the control of Scer\GAL4en-e16E generate few filopodia and smooth, but smaller, lamellipodia than wild type.
No neuromuscular junction defects are detectable in larvae expressing Zzzz\actAFP4mito.Scer\UAS.T:Avic\GFP-EGFP under the control of Scer\GAL4how-24B.
Embryos expressing Zzzz\actAFP4mito.Scer\UAS.T:Avic\GFP-EGFP under the control of Scer\GAL4e22c have reduced longitudinal axons in the central nervous system.
Embryos expressing Zzzz\actAFP4mito.Scer\UAS.T:Avic\GFP-EGFP under the control of Scer\GAL4elav.PLu show an ISNb bypass phenotype in 88% of segments.
Embryos expressing Zzzz\actAFP4mito.Scer\UAS.T:Avic\GFP-EGFP under the control of Scer\GAL4e22c have deep segmental grooves and an uneven leading edge during dorsal closure. There are severe abnormalities in epithelial zippering during dorsal closure; dorsal openings are oval rather than almond-shaped and leading edges sometimes meet in the middle before zippering has occurred. As a result, migration is 2.2-fold slower than wild type, with much of the delay in late epithelial zippering.
68% of embryos expressing Zzzz\actAFP4mito.Scer\UAS.T:Avic\GFP-EGFP under the control of Scer\GAL4e22c have a wild-type cuticle, while 30% show misalignment/puckering along the dorsal midline.
Embryos derived from females expressing Zzzz\actAFP4mito.Scer\UAS.T:Avic\GFP-EGFP under the control of Scer\GAL4mat.αTub67C.T:Hsim\VP16 proceed through gastrulation normally and have normal epithelial integrity. Defects in attachment of amnioserosa and epidermal cells is seen, both prior to germband retraction and most obviously after retraction begins. Segmental grooves are deeper than normal in these embryos and persist long after they should have regressed. The leading edge during dorsal closure is often uneven. Most of the embryos fail in head involution. Cells that should lead head involution appear to constrict far more than in wild type, nearly severing the head from the thorax.
79% of embryos derived from females expressing Zzzz\actAFP4mito.Scer\UAS.T:Avic\GFP-EGFP under the control of Scer\GAL4mat.αTub67C.T:Hsim\VP16 die. The mature embryos show cuticle defects; 8% have a dorsal pucker, 18% have a hole in the head, 22% have both a dorsal pucker and a hole in the head, 39% have defects in germband retraction and 9% have a ventral hole.
Larvae expressing Zzzz\actAFP4mito.Scer\UAS.T:Avic\GFP-EGFP under the control of Scer\GAL4en-e16E show no detectable defects in epithelial architecture of the imaginal discs.
Leading edge cells in embryos expressing Zzzz\actAFP4mito.Scer\UAS.T:Avic\GFP-EGFP under the control of Scer\GAL4en-e16E produce lamellipodia, but produce only rare, very short filopodia, with both the number of filopodia and the average length of a filopodium being reduced compared to wild type.
Lmon\actAFP4mito.UAS.EGFP/Scer\GAL415J2 is an enhancer of abnormal neuroanatomy | recessive phenotype of Nl1N-ts1
Lmon\actAFP4mito.UAS.EGFP/Scer\GAL4how-24B is a suppressor of abnormal neuroanatomy | third instar larval stage phenotype of mir-8Δ
Lmon\actAFP4mito.UAS.EGFP/Scer\GAL4how-24B is a suppressor of abnormal neuroanatomy phenotype of mir-8Δ2
Lmon\actAFP4mito.UAS.EGFP has egg | maternal effect phenotype, suppressible by cpb1/cpb[+]
Lmon\actAFP4mito.UAS.EGFP has egg | maternal effect phenotype, suppressible by Abl4/Abl[+]
Lmon\actAFP4mito.UAS.EGFP/Scer\GAL415J2 is an enhancer of pioneer neuron phenotype of Nl1N-ts1
Lmon\actAFP4mito.UAS.EGFP/Scer\GAL4how-24B is a suppressor of subsynaptic reticulum | third instar larval stage phenotype of mir-8Δ
Lmon\actAFP4mito.UAS.EGFP, Scer\GAL4en-e16E is a suppressor of filopodium phenotype of Scer\GAL4en-e16E, diaFH1FH2.UASp.EGFP
Lmon\actAFP4mito.UAS.EGFP, Scer\GAL4en-e16E is a suppressor of embryonic leading edge cell phenotype of Scer\GAL4en-e16E, diaFH1FH2.UASp.EGFP
Lmon\actAFP4mito.UAS.EGFP, Scer\GAL4en-e16E is a suppressor of lamellipodium phenotype of Scer\GAL4en-e16E, diaFH1FH2.UASp.EGFP
Lmon\actAFP4mito.UAS.EGFP/Scer\GAL4how-24B is a suppressor of embryonic/larval neuromuscular junction | third instar larval stage phenotype of mir-8Δ2
Lmon\actAFP4mito.UAS.EGFP/Scer\GAL4how-24B is a suppressor of NMJ bouton | larval stage phenotype of mir-8Δ2
Lmon\actAFP4mito.UAS.EGFP, Scer\GAL4en-e16E is a non-suppressor of filopodium | ectopic phenotype of Scer\GAL4en-e16E, diaΔDad.UASp.EGFP
Lmon\actAFP4mito.UAS.EGFP, Scer\GAL4en-e16E is a non-suppressor of epidermal cell phenotype of Scer\GAL4en-e16E, diaΔDad.UASp.EGFP
Lmon\actAFP4mito.UAS.EGFP, Scer\GAL4en-e16E is a non-suppressor of embryonic leading edge cell phenotype of Scer\GAL4en-e16E, diaΔDad.UASp.EGFP
Expression of Zzzz\actAFP4mito.Scer\UAS.T:Avic\GFP-EGFP under the control of Scer\GAL415J2 enhances the early longitudinal axon phenotype of Nl1N-ts1.
The penetrance of the "dumpless" phenotype seen in eggs derived from females expressing Zzzz\actAFP4mito.Scer\UAS.T:Avic\GFP-EGFP is partially suppressed by cpb1/+ or Abl4/+.
Co-expression of Zzzz\actAFP4mito.Scer\UAS.T:Avic\GFP-EGFP under the control of Scer\GAL4en-e16E does not suppress the ability of diaΔDad.Scer\UAS.P\T.T:Avic\GFP-EGFP to induce elevated numbers of filopodia on leading edge cells or on more ventral epidermal cells. The lifetime of the filopodia is still longer than normal in the co-expressing embryos. The number of lamellipodia and lamellipodial area is significantly reduced in the co-expressing leading edge cells compared to wild type.
Co-expression of Zzzz\actAFP4mito.Scer\UAS.T:Avic\GFP-EGFP largely restores filopodia number and length to wild type in leading edge cells expressing diaFH1FH2.Scer\UAS.P\T.T:Avic\GFP-EGFP under the control of Scer\GAL4en-e16E. Fewer ruffle-like lamellipodia are seen and those that form are nearer wild type in size.
Expression of Zzzz\actAFP4mito.Scer\UAS.T:Avic\GFP-EGFP under the control of Scer\GAL4how-24B rescues the neuromuscular junction phenotypes seen in mir-8Δ2 larvae.
