cell body & serotonin neuron
serotonin neuron & ventral nerve cord
leaX123 embryos show much milder defects compared to robo4, leaX123 double mutant embryos: 29% of leaX123 embryos have one or more pericardial cells that migrate too far dorsally and are found closer to the dorsal midline in front of the rows of cardioblasts. leaX123 embryos also occasionally display alignment defects in the rows of cardioblasts, although gaps between cardioblasts are not apparent.
Ventral nerve cords from stage 16 leaX123/leaX123 embryos show a random loss of ability to take up serotonin in approximately half of hemisegments. The cell bodies of serotonergic neurons in the ventral nerve cord of stage 16 leaX123/leaX123 embryos are shifted towards the midline compared to wild-type.
Mutant embryos do not show defects in the position of the vmd1a neuron of the ventral multidendritic neuron cluster in the abdomen; a single vmd1a neuron is seen in each hemisegment.
Homozygous larvae have no detectable defect in distal cell neuron positioning in the visual system.
robo2X123/robo2x135 is an enhancer of abnormal neuroanatomy phenotype of fra3/fra4
Scer\GAL4Mef2.PR, robo2UAS.cSa, robo2X123 has dorsal vessel wall cell | ectopic phenotype, enhanceable by robo14
robo2X123 has serotonin neuron & ventral nerve cord phenotype, suppressible by egUAS.cDa/Scer\GAL4eg-Mz360
robo2X123/robo2x135 is an enhancer of symmetrical commissure phenotype of fra3/fra4
robo2X123/robo2x135 is an enhancer of larval EW neuron phenotype of fra3/fra4
robo11, robo2X123 has germinal proliferation center | embryonic stage 17 phenotype
Scer\GAL4Mef2.PR, robo14, robo2UAS.cSa, robo2X123 has dorsal vessel wall cell phenotype
robo14, robo2X123 has dorsal vessel wall cell phenotype
robo14, robo2X123 has embryonic pericardial cell phenotype
robo11, robo2X123 has muscle cell of A1-7 ventral longitudinal muscle 3 phenotype
Embryos mutant for both robo4 and leaX123 show defects in cardioblast and pericardial cell positioning and alignment, similar to slit2 embryos. The number of cardioblast nuclei that reach the dorsal midline in these embryos is approximately 86.2, compared to approximately 104 in wild type embryos.
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.
In the ventral nerve cords of stage 16 leaX123/leaX123 embryos, the number of hemisegments showing loss of ability to take up serotonin is not significantly increased by egMz360/egMz360. The loss of serotonin uptake activity and the serotonergic axon guidance phenotypes of leaX123/leaX123 embryos are suppressed by egScer\UAS.cDa; Scer\GAL4eg-Mz360.
robo1 leaX123 double mutant embryos show defects in the position of the vmd1a neuron of the ventral multidendritic neuron cluster in the abdomen; in 21% of segments loss of the vmd1a neuron in a hemisegment is associated with duplication of the vmd1a neuron in the contralateral hemisegment. In addition, in 36% of segments, some vmd1a neurons are missing from the ventral vmd clusters (in most of these segments, the missing md neurons are probably located near the midline).
87% of segments show crossing of the midline by muscles 6/7 in robo1 leaX123 double mutant embryos. This defect is rescued by expression of roboScer\UAS.cKa under the control of Scer\GAL4how-24B, but the axonal phenotype of these embryos is mutant. 1% of segments show crossing of the midline by muscles 6/7, 5% show abnormal insertion of muscle 5 and 3% show abnormal insertion of muscles 6/7 in sli2 leaX123 double mutant embryos. 15% of segments show crossing of the midline by muscles 6/7, 31% show abnormal insertion of muscle 5 and 16% show abnormal insertion of muscles 6/7 in sli2 robo1 leaX123 triple mutant embryos.