The fluorescent tag is appended to the N-terminus of ena.
filopodium & embryonic leading edge cell, with Scer\GAL4en-e16E
Border cell clusters expressing enaScer\UAS.T:Avic\GFP under the control of Scer\GAL4slbo.2.6 have many fine protrusions at the beginning of migration, in contrast to wild type, where one prominent protrusion is usually seen in the direction of the oocyte. Border cell migration is defective in these mutants.
Expression of enaScer\UAS.T:Avic\GFP under the control of Scer\GAL4en-e16E can increase filopodia number and length at the leading edge and larger lamellipodia are seen.
Expression of enaScer\UAS.T:Avic\GFP under the control of Scer\GAL4e22c does not result in embryonic lethality.
Leading edge cells in embryos expressing enaScer\UAS.T:Avic\GFP under the control of Scer\GAL4en-e16E produce longer filopodia than wild type. Lateral epithelial cells produce many filopodia in these embryos (these cells do not produce filopodia in wild-type embryos).
enaUAS.GFP/Scer\GAL415J2 is a suppressor of abnormal neuroanatomy | recessive phenotype of Nl1N-ts1
enaUAS.GFP/Scer\GAL415J2 is a suppressor of pioneer neuron phenotype of Nl1N-ts1
Scer\GAL4en-e16E, diaΔDad.UASp.EGFP, enaUAS.GFP has embryonic leading edge cell phenotype
Scer\GAL4en-e16E, diaΔDad.UASp.EGFP, enaUAS.GFP has filopodium phenotype
Scer\GAL4en-e16E, diaΔDad.UASp.EGFP, enaUAS.GFP has lamellipodium phenotype
Scer\GAL4en-e16E, diaΔDad.UASp.EGFP, enaUAS.GFP has epidermal cell phenotype
Scer\GAL4en-e16E, diaDDFH1FH2.UASp.EGFP, enaUAS.GFP has embryonic leading edge cell phenotype
Scer\GAL4en-e16E, diaDDFH1FH2.UASp.EGFP, enaUAS.GFP has filopodium phenotype
Scer\GAL4en-e16E, diaDDFH1FH2.UASp.EGFP, enaUAS.GFP has lamellipodium phenotype
Scer\GAL4en-e16E, diaFH1FH2.UASp.EGFP, enaUAS.GFP has embryonic leading edge cell phenotype
Scer\GAL4en-e16E, diaFH1FH2.UASp.EGFP, enaUAS.GFP has filopodium phenotype
Scer\GAL4en-e16E, diaFH1FH2.UASp.EGFP, enaUAS.GFP has lamellipodium phenotype
Expression of enaScer\UAS.T:Avic\GFP under the control of Scer\GAL415J2 suppresses the early longitudinal axon phenotype of Nl1N-ts1.
Co-expression of enaScer\UAS.T:Avic\GFP and diaΔDad.Scer\UAS.P\T.T:Avic\GFP-EGFP under the control of Scer\GAL4en-e16E in embryos induces protrusions in epidermal cells that are different from those produced by expression of either construct alone. Co-expression results in lamellipodia both at the leading edge and in more ventral epidermal cells, at the expense of filopodia.
Co-expression of enaScer\UAS.T:Avic\GFP and diaDDFH1FH2.Scer\UAS.P\T.T:Avic\GFP-EGFP under the control of Scer\GAL4en-e16E in embryos results in fewer filopodia but larger lamellipodia at the leading edge.
Co-expression of enaScer\UAS.T:Avic\GFP and diaFH1FH2.Scer\UAS.P\T.T:Avic\GFP-EGFP under the control of Scer\GAL4en-e16E in embryos results in fewer filopodia but larger lamellipodia at the leading edge.
enaUAS.GFP/Scer\GAL4how-24B partially rescues enaGC5