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General Information
D. melanogaster
FlyBase ID
Feature type
Associated gene
Associated Insertion(s)
Carried in Construct
Nature of the Allele
Mutations Mapped to the Genome
Additional Notes
point mutation
Nucleotide change:


Amino acid change:

R902term | robo2-PA; R902term | robo2-PB

Reported amino acid change:



Site of nucleotide substitution in mutant inferred by FlyBase based on reported amino acid change.

Associated Sequence Data
DNA sequence
Protein sequence
Progenitor genotype
Nature of the lesion

Amino acid replacements are a revision of the data reported in FBrf0132258. They are numbered relative to the 1406 amino acid residue predicted protein.

Amino acid replacement: R845term.

Expression Data
Reporter Expression
Additional Information
Marker for
Reflects expression of
Reporter construct used in assay
Human Disease Associations
Disease Ontology (DO) Annotations
Models Based on Experimental Evidence ( 0 )
Modifiers Based on Experimental Evidence ( 0 )
Comments on Models/Modifiers Based on Experimental Evidence ( 0 )
Phenotypic Data
Phenotypic Class
Phenotype Manifest In
Detailed Description

learobo2-8/lea2 stage 13 embryos have gonads with unfused somatic gonadal precursor (SGP) clusters. By stage 15, SGP clusters fuse but gonads then fail to compact properly. Mutants also show germ cell ensheathment defects.

learobo2-8/learobo2-4 stage 13 embryos have gonads with unfused somatic gonadal precursor (SGP) clusters. By stage 15, SGP clusters fuse but gonads then fail to compact properly. Mutants also show germ cell ensheathment defects.

Fas2-positive longitudinal axons show a number of defects in learobo2-4/learobo2-8 stage 16 embryos; Fas2-positive axons extend across or along the midline in 23.7% of segments, intermediate Fas2-positive fascicles are fused or broken in 10.2% of hemisegments and lateral Fas2-positive fascicles are fused or broken in 29.9% of hemisegments.

There are no significant defects in abdominal cluster dendritic branching in animals mutant for learobo2-8.

The dendrite morphology of class I and class IV neurons is normal in learobo2-8 single cell mutant clones.

Subtle myocardial cell alignment defects are observed in learobo2-8 stage 16 embryos.

In embryonic stage 16 learobo2-8 mutants, axons defasciculate and longitudinal glia are disorganised, although the phenotype is rather weak (26% penetrance) and the glia do not migrate abnormally close to the midline.

The lch5 axons are stalled, most frequently before turning point TP1 but sometimes between turning points TP1 and TP2, in 1% of hemisegments in mutant embryos. Stalling is also seen in dorsal cluster axons in about 1% of thoracic and abdominal hemisegments, but the most common defect in the dorsal cluster axons is projection in aberrant directions in 5-7% of hemisegments.

6% of ganglionic branches cross the midline in learobo2-4/learobo2-8 embryos and 15% of ganglionic branches fail to enter the central nervous system. 18% of dorsal tracheal branches are stalled or missing and 30% of the remaining branches fail to fuse over the heart.

Homozygous embryos show defects in the Fas2-expressing fascicles. 8.5% of embryos show fusion between the medial and intermediate fascicles, 23.0% show fusion between the lateral and intermediate fascicle, 4.7% show breaks in the intermediate fascicle and 15.2% show breaks in the lateral fascicle.

In robo8 homozygous mutants about a quarter of Fas2 positive axons in the ventral nerve cord are misrouted. These form bundles of varying thickness.

External Data
Show genetic interaction network for Enhancers & Suppressors
Phenotypic Class
Enhanced by

lea[+]/robo28, robo11 has neuroanatomy defective | recessive phenotype, enhanceable by captk01217/capt[+]

Enhancer of

robo28 is an enhancer of neuroanatomy defective phenotype of chb4, robo11

Phenotype Manifest In
Enhanced by
NOT Enhanced by
Suppressed by
Enhancer of

robo28 is an enhancer of cardioblast phenotype of robo11

robo28 is an enhancer of embryonic/larval neuron phenotype of chb4, robo11

NOT Enhancer of
NOT Suppressor of
Additional Comments
Genetic Interactions

learobo2-8/+ fails to suppress the dorsal branch fusion phenotype seen when SdcdsRNA.Scer\UAS.cSa is expressed under the control of Scer\GAL4btl.PS.

Many of the dorsal abdominal clusters in robo1/learobo2-8 mutant animals have branches that exceed the normal level of extension at approximately 21 and 22 hours after egg laying, but this phenotype is not significantly greater than the defects observed in robo1 mutants.

robo1, learobo2-8 double mutants show severe myocardial cell misalignment including gaps, intercalation, and double rows.

learobo2-8 enhances the defects in dorsal branch formation seen in stumpsems7 embryos; in the double mutant 71% are missing and 8% are stalled.

Heterozygosity for learobo2-8 enhances the frequency of axons ectopically crossing the midline that is seen in robo1 chb4 double heterozygous embryos. robo1 learobo2-8 double heterozygous embryos have axons ectopically crossing the midline.

robo1 learobo2-8 double mutant embryos show misprojection of lch5 axons to the v'ch1 axon pathway in 11% of hemisegments (a similar frequency to robo1 single mutants). Stalling of the lch5 axons prior to turning point TP2, a characteristic of the learobo2-8 single mutant, is also seen in double mutant embryos, although at a higher frequency (6% of hemisegments). The dorsal cluster misprojection phenotype seen in learobo2-8 single mutant embryos is not seen in the robo1 learobo2-8 double mutant embryos; in the double mutant embryos the dorsal cluster axons follow a normal trajectory to the lateral region, although in 7% of hemisegments they grow abnormally from this point, either projecting along the v'ch1 route or growing intersegmentally. The lch5 cell bodies are located dorsal to their normal position in 11% of hemisegments and are aberrantly oriented in 3% of hemisegments of robo1 learobo2-8 double mutant embryos. Missing or aberrantly positioned spiracular branches and failure of motor axons to extend as far as the sensory neuron cluster are occasionally seen.

Expression of roboScer\UAS.T:Ivir\HA1,T:wg under the control of Scer\GAL4bs.Term partially rescues the failure of ganglionic branches to enter the central nervous system that is seen in learobo2-4/learobo2-8 embryos and the weak midline crossing phenotype of the ganglionic branches seen in these embryos is also rescued. Expression of sliScer\UAS.cKa under the control of Scer\GAL4twi.PG in a learobo2-8 background does not result in any new tracheal branches growing from trunk metameres T2 to T9.

One copy of captk01217 enhances the frequency of midline crossing defects seen in robo1 learobo2-8 double mutant heterozygotes.

Xenogenetic Interactions
Complementation and Rescue Data
Images (0)
Stocks (0)
Notes on Origin
External Crossreferences and Linkouts ( 0 )
Synonyms and Secondary IDs (3)
References (17)