Expression of leaScer\UAS.cSa in cardioblasts using Scer\GAL4Mef2.PR results in a lateral shift of the row of cardioblasts away from the dorsal midline to a position normally occupied by pericardial cells in approximately 84% of embryos: the distance between opposing cardioblast nuclei in these embryos (at stage 16) is approximately 22.28 μm compared to approximately 9.21 μm in stage 16 wild type embryos. This abnormal space between the cardioblast rows is maintained through stage 17 when the opposing pairs of cells should have fused at the midline. Although the cardioblast rows are displaced laterally in leaScer\UAS.cSa-expressing cells, there are no visible gaps between the cardioblasts, indicating that adhesion between these cells is maintained.
Expression of leaScer\UAS.cSa, in the giant fiber axons, under the control of Scer\GAL4A307 results in a strong deflection of the fibers in the posterior regions of T1 and T2. Expression of leaScer\UAS.cSa, under the control of Scer\GAL4A307 does not affect the latency of the giant fiber, with only subtle defects in following frequency. Even with two copies of leaScer\UAS.cSa, no physiological latency effect is found.
Expression of leaScer\UAS.cSa under the control of Scer\GAL4GMR.PF has no effect on retinal patterning.
Expression of leaScer\UAS.cSa under the control of Scer\GAL4how-24B results in guidance defects in muscles 21 through 23, but no other significant muscle patterning defects.
Expression of leaScer\UAS.cSa under the control of Scer\GAL4elav.PLu results in a comm-like phenotype. All three Fas2-expressing longitudinal bundles are compressed into a single fascicle.
With a low and increasing level of lea overexpression results in a inappropriate midline crossing. As levels of lea continue to increase, the response becomes biphasic. The proclivity to cross the midline is replaced at higher levels (e.g when driven by Scer\GAL4elav.PLu) by an increased tendency to avoid the midline leading to a commissureless phenotype. The overexpression of leaScer\UAS.cSa in all neurons in a leaunspecified background causes much more severe disruptions in axon pathfinding than in leaunspecified embryos alone. CNS axons are observed leaving the CNS; some of them return into the CNS several segments later. Motor axons in the periphery cross over segment boreders and ectopically fasciculate, sometimes with axons from several segments away. The medial, intermediate, and lateral Fas2 longitudinal pathways fasciculate together and travel back and forth across the midline repeatedly. This genotype results in a more disorganised axon scaffold than does leaScer\UAS.cSa overexpression in a wild-type background.
Scer\GAL4shakB.lethal.4.1, robo2UAS.cSa has abnormal neuroanatomy phenotype, suppressible by Scer\GAL4shakB.lethal.4.1/commΔC.UAS
Scer\GAL4shakB.lethal.4.1, robo2UAS.cSa has abnormal neurophysiology phenotype, suppressible by Scer\GAL4shakB.lethal.4.1/commΔC.UAS
Scer\GAL4shot-OK307, robo2UAS.cSa has abnormal neuroanatomy phenotype, suppressible by commUAS.cKa/Scer\GAL4shot-OK307
robo2UAS.cSa is an enhancer of visible phenotype of AblUAS.cFa, Scer\GAL4GMR.PF
Scer\GAL4Mef2.PR, robo2UAS.cSa, robo2X123 has dorsal vessel wall cell | ectopic phenotype, enhanceable by robo14
Scer\GAL4Mef2.PR, robo2UAS.cSa has dorsal vessel wall cell | ectopic phenotype, non-enhanceable by robo14
Scer\GAL4shakB.lethal.4.1, robo2UAS.cSa has giant fiber neuron phenotype, suppressible by Scer\GAL4shakB.lethal.4.1/commΔC.UAS
Scer\GAL4shot-OK307, robo2UAS.cSa has giant fiber neuron phenotype, suppressible by commUAS.cKa/Scer\GAL4shot-OK307
Scer\GAL4elav.PLu, robo2UAS.cSa has larval ventral nerve cord commissure phenotype, suppressible | partially by robo11
Scer\GAL4elav.PLu, robo2UAS.cSa has larval ventral nerve cord commissure phenotype, suppressible | partially by robo15/robo11
Scer\GAL4elav.PLu, robo2UAS.cSa has larval ventral nerve cord commissure phenotype, suppressible | partially by sli2
Scer\GAL4elav.PLu, robo2UAS.cSa has larval ventral nerve cord commissure phenotype, suppressible | partially by enaGC1
Scer\GAL4Mef2.PR, robo2UAS.cSa has dorsal vessel wall cell | ectopic phenotype, non-suppressible by robo14
robo2UAS.cSa is an enhancer of ommatidium phenotype of AblUAS.cFa, Scer\GAL4GMR.PF
Scer\GAL4Mef2.PR, robo14, robo2UAS.cSa has embryo | dorsal closure stage phenotype
Expression of leaScer\UAS.cSa in cardioblasts using Scer\GAL4Mef2.PR in a robo4 mutant background results in similar defects as when leaScer\UAS.cSa is expressed using Scer\GAL4Mef2.PR in an otherwise wild type background. Namely, a lateral shift of the row of cardioblasts away from the dorsal midline to a position normally occupied by pericardial cells while adhesion between these cells is maintained.
Embryos expressing leaScer\UAS.cSa under the control of Scer\GAL4Mef2.PR in a robo4, leaX123 double mutant background display gaps in rows of cardioblasts indicating a loss of adhesion between cardioblasts (as seen in robo4, leaX123 double mutants) as well as the mispositioning of these cells away from the dorsal midline (as seen in leaScer\UAS.cSa, Scer\GAL4Mef2.PR embryos).
Embryos expressing leaScer\UAS.cSa under the control of Scer\GAL4Mef2.PR in a robo4, leaX123 double mutant background exhibit mispositioning of cardioblasts away from the dorsal midline which is more severe as compared to expression of leaScer\UAS.cSa using Scer\GAL4Mef2.PR in an otherwise wild type background; cardioblasts are displaced even more laterally, with cardioblasts and pericardial cells even being observed in somatic muscle territory.
Expression of leaScer\UAS.cSa under the control of Scer\GAL4Mef2.PR in a robo4 mutant background results in a slight delay in dorsal closure: a slight gap between dorsal ectodermal cells is seen in late stage mutant embryos that is not observed in wild type embryos.
The lateral shifts in the giant fibers induced by overexpression of leaScer\UAS.cSa, under the control of Scer\GAL4A307 can be suppressed by co-overexpression of commScer\UAS.cKa with Scer\GAL4A307. Co-expression of one copy of commΔC.Scer\UAS, under the regulation of Scer\GAL4shakB.lethal.4.1, is able to rescue the anatomical and physiological effect of one or two copies of leaScer\UAS.cSa.
Co-expression of leaScer\UAS.cSa enhances the rough eye phenotype caused by expression of AblScer\UAS.cFa under the control of Scer\GAL4GMR.PF.
The commissureless phenotype seen when leaScer\UAS.cSa is driven by Scer\GAL4elav.PLu, is partially suppressed by the addition of enaGC1/+, robo1/+, robo1/robo5 or sli2/+. Although the number of commissure that form in these backgrounds is increased, the phenotype is more complex than simple suppression because in many cases the crossovers that now occur are inappropriate.