The adult sLNv neurons of robo11
transheterozygotes do not show significant axon length differences compared to controls.
homozygous embryonic heart cardioblasts show a rounded morphology, show significant decreases in migration velocity, as well as in filopodial and lamellopodial extensions and activities, as compared to controls; these defects are associated with embryonic heart lumen formation defects, as compared to controls. robo11
heterozygous cardioblasts also show a significant decrease in migration velocity, filopodial activity and lamellopodial activity, as compared to controls.
homozygous embryos display defects in midline repulsion leading to axons ectopically crossing the ventral nerve cord midline.
, but not robo11
/+, mutant embryos exhibit ventral nerve cord defects, including axon guidance defects, with FasII-positive axons crossing the midline in every segment, and the pCC neuron inappropriately extends across the midline, in contrast to wild type.
Axons from the medial Fas2
-positive pathway cross the line in every segment in mutant embryos.
embryos exhibit gonad compaction defects and germ cell ensheathment defects.
mutants, the medial Fas2
-positive axon tracts ectopically cross and recross the midline. The axons expressing Scer\GAL4ap-md544
also collapse along the midline and follow the medial Fas2
-positive longitudinal axons show repeated crossing of the midline in robo1
stage 16 embryos.
99.1% of segments have Fas2
-positive axons extending across or along the midline in stage 16-17 homozygous embryos.
mutant embryos display a phenotype where axons repeatedly cross the midline in a circular fashion.
Single cell robo1
leg motoneuron clones induced 48 hr after hatching have the following phenotypes: the posterior dendritic branch crosses the midline at the same site as it does in wild type clones, but there are ectopic branches the that extend toward the midline at more anterior positions within the neuropil; more of the dendritic arborization is found in the medial territory than controls; the mean centre of mass is shifted toward the midline compared to controls; the mean 33rd percentile of arborization is shifted towards the midline.
Single cell robo1
leg motoneuron clones induced 96 hr after hatching have the following phenotypes: a shift in the distribution of dendrites toward the midline; the mean centre of mass shifts towards the midline compared to controls; the mean 33rd percentile of arborization shifts towards the midline. There is no evidence for a disruption to the axonal projections of clones to the periphery. In a dorsoventral plane, these clones show a shift of dendrites towards the posterior neuropil and a slight loss in the ventral neuropil.
mutants exhibit an ectopic midline innervation phenotype (with 100% penetrance for MN-LL1 and 89% penetrance for MN-DA3).
mutants exhibit axon guidance defects whereby the commissural axons cross the midline repetitively to give characteristic 'roundabouts'.
heterozygous mutants appear wild-type.
Many of the dorsal abdominal clusters in robo1
mutant animals have branches that exceed the normal level of extension at approximately 21 and 22 hours after egg laying. The maximal dendrite length with respect to the most dorsally positioned neuronal cell body is significantly altered in mutants.
Class IV robo1
mutant neurons display dendrite over-elongation and reduced branching. Class IV neurons show less high order branches and form longer dendrite process compared to control embryos. The number of branches of class IV neurons is significantly decreased in robo1
mutants at 22 hours after egg laying. The dorsal elongation and the average branch length are significantly increased.
Class I neurons in robo1
mutant embryos do not show any defects in dendrite branch length or number compared to control embryos.
single cell mutant class IV neurons have less high order branches than control clones. The number of quaternary and higher order branches is less than half compared to controls. The average length of all branch orders is unchanged.
single cell mutant clones of either two dorsal class I neurons display normal dendrite morphology.
embryos show an axon guidance defect of the Apterous neurons with neurons aberrantly crossing the midline. robo1
Apterous neurons exhibit these crossing defects during the initial extension toward the midline and throughout development.
Medial axon bundles abnormally cross and re-cross the midline in homozygous robo1
mutant embryos present a fused commissure phenotype in 100% of neuromeres.
The initial lateral projection and posterior turn of the dMP2 and MP1 pioneer neurons are normal in developing mutant embryos. The axons fasciculate as in wild type and extend their axons posteriorly. When they reach the commissure of the next segment, MP1 crosses the commissure and follows the correct longitudinal pathway. However, most dMP2 axons show an abnormal trajectory at this point, separating from the MP1 axon, tracking the commissural axons and crossing the midline (rather than following a longitudinal pathway as in wild type).
The normal anterior projections of the pCC and vMP2 neurons are misdirected contralaterally in mutant embryos.
embryos show weak salivary gland guidance defects.
Subtle myocardial cell alignment defects are observed in learobo2-8
stage 16 embryos.
embryos there is ectopic midline crossing of most CNS axons, and disorganized and inappropriate serotonergic neuron branching towards the midline. Despite their defects in serotonergic neuronal axon guidance, these neurons retain their normal ability to take up serotonin.
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.
About 26-40% of heterozygous robo1
stage 16 embryos exhibit axon bundles that cross the midline incorrectly.
Homozygous embryos show sensory axon defects; one or more axons from the lch5 cluster project inappropriately to join the v'ch1 axon or the v' cluster in 10% of hemisegments. In these hemisegments, the remaining lch5 axons project in a normal fashion to the intersegmental nerve. In addition, the axon of one of the lesA and ldaA neurons (usually the lesA neuron) follows the v'ch1 pathway in 23% of hemisegments. Occasionally (3% of hemisegments), v'ch1 or other v' cluster axons grow dorsally before turning back into the segmental nerve or inappropriately joining the intersegmental nerve. No defects are seen in the dorsal trunk, transverse connective or visceral branch.
The terminal branches of the dbd neurons generally cross the midline and often form mirror image bilateral projections. The projections retain their association with the medial Fas2
fascicle. Approximately half of the time the terminal branches of the ch neurons have a branch crossing the midline. The projections retain their association with the intermediate Fas2
/+ embryos, midline crossovers are seen in the pCC/MP2 pathway axons in 25% of embryos. An average of 1.1 crossovers are seen per embryo.
One or two Fas2
-positive axon bundles cross the midline in about 26% of heterozygous embryos.
/+ heterozygous mutant embryos exhibit midline crossing at a frequency of ~4.8%.
43% of heterozygous embryos show abnormal midline crossing of axons.
5% of segments show crossing of the midline by muscles 6/7, 11% show abnormal insertion of muscle 5 and 15% show abnormal insertion of muscles 6/7 in mutant embryos.
Approximately 53% of heterozygous embryos show periodic crossovers of Fas2
-positive axons across the midline.
mutant embryos all of the innermost fascicles from each side of the midline combine to form a single thick bundle that meanders back and forth along the midline.
The inner Fas2
-positive longitudinal bundle crosses the midline and circles around it in the central nervous system of homozygous embryos.
Embryos heterozygous for either robo1
show deviation of longitudinal fascicles towards the midline in less than 5% of segments.
-expressing interneurons cross the midline in every segment in homozygous embryos, join up with their contralateral homologues, and often project anteriorly in one discrete longitudinal fascicle. In heterozygous embryos 5% of all ap
-expressing axons cross the midline.
Mutant phenotype of lateral chordotonal axons includes: shorter axons or defasciculated axons.
"Fuzzy commisure" phenotype in embryonic central nervous system.