Expression of Src64BYF.Scer\UAS under the control of Scer\GAL4pros.PMG induces extreme nephrocyte agglutination and severe loss of filtration diaphragms. No apoptosis is evident. Dramatic changes in nephrocyte organisation are seen; the cells lack a cortical region due to the absence of labyrinthine channels and filtration diaphragms, the organelles appear close to the membrane, the basement membrane is thicker with occasional inclusions and the cytoplasm contains intracellular structures composed of membrane fragments. Furthermore there are membranes separating adjacent nephrocytes with regions rich in adherens junctions.
When Src64BYF.Scer\UAS is expressed in nephrocytes under the control of Scer\GAL4pros.PMG and restricted to a ten hour period beginning at the third instar larval stages (using Scer\GAL80ts.αTub84B), nephrocyte damage is seen. Strong nephrocyte agglutination and loss of filtration diaphragms are seen. Filtration diaphragm integrity is substantially improved 24 hours later and complete after another 24 hours.
Expression of Src64BYF.Scer\UAS in EW neurons under the control of Scer\GAL4eg-Mz360, has no effect in wild-type embryos.
Females that express the Src64BYF.Scer\UAS transgene under the control of Scer\GAL4nos.UTR.T:Hsim\VP16 do not show ring canal size defects. However, these females do show egg chamber packaging defects. Additionally, cysts with aberrant cell numbers are frequently observed in Scer\GAL4nos.UTR.T:Hsim\VP16>Src64BYF.Scer\UAS germaria. There is a higher penetrance of packaging defects in germaria versus vitellaria.
When Src64BYF.Scer\UAS is driven by Scer\GAL4GMR.PF, a range of phenotypes is seen in the eye in an insertion, dose dependent and temperature sensitive manner. These range through lethality, a complete loss of the eye, to small rough eyes. When the developing eye disc is examined, ectopic proliferation of uncommitted cells (which usually arrest in G1/G0) in the disc is seen. Mutant eye discs also exhibit increased cell death, displaying a stronger effect than Src64BScer\UAS.cPa.
Scer\GAL4GMR.PF, Src64BYF.UAS has increased cell death phenotype, non-suppressible by CskUAS.cPa, Scer\GAL4GMR.PF
Scer\GAL4GMR.PF, Src64BYF.UAS has increased occurrence of cell division | larval stage phenotype, non-suppressible by CskUAS.cPa, Scer\GAL4GMR.PF
Scer\GAL4eg-Mz360/Src64BYF.UAS is an enhancer of abnormal neuroanatomy phenotype of fra6/fra3
Scer\GAL4eg-Mz360/Src64BYF.UAS is an enhancer of abnormal neuroanatomy phenotype of Scer\GAL4eg-Mz360, fraΔC.UAS.Tag:HA
Scer\GAL4GMR.PF, Src64BYF.UAS has eye phenotype, non-suppressible by CskUAS.cPa, Scer\GAL4GMR.PF
Scer\GAL4eg-Mz360/Src64BYF.UAS is an enhancer of larval EW neuron phenotype of fra6/fra3
Scer\GAL4eg-Mz360/Src64BYF.UAS is an enhancer of larval posterior commissure phenotype of fra6/fra3
Scer\GAL4eg-Mz360/Src64BYF.UAS is an enhancer of larval longitudinal connective phenotype of fra6/fra3
Scer\GAL4eg-Mz360/Src64BYF.UAS is an enhancer of larval EW neuron phenotype of Scer\GAL4eg-Mz360, fraΔC.UAS.Tag:HA
Scer\GAL4eg-Mz360/Src64BYF.UAS is an enhancer of symmetrical commissure phenotype of Scer\GAL4eg-Mz360, fraΔC.UAS.Tag:HA
Co-expression of Src64BYF.Scer\UAS under the control of Scer\GAL4eg-Mz360 enhances the EW axon midline crossing defects found in fra3/fra6 hypomorphic mutants.
Co-expression of Src64BYF.Scer\UAS with fraΔC.Scer\UAS.T:Ivir\HA1 in eg-expressing neurons, under the control of Scer\GAL4eg-Mz360 enhances the midline crossing defects found when fraΔC.Scer\UAS.T:Ivir\HA1 alone is expressed under the control of Scer\GAL4eg-Mz360.