|Feature type||allele||Associated gene||Dmel\lea|
|Also Known As||robo28|
|Map ( GBrowse )|
|Allele class||loss of function allele|
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|Nature of the Allele|
|Mutations Mapped to the Genome|
|Associated Sequence Data|
|Nature of the lesion|
Amino acid replacement: R845@ (revision of data in FBrf0132258). Amino acid replacements are relative to the 1406 amino acid residue predicted protein.
Amino acid replacement: R902@. See Dickson, 2001.3.14, personal communication for subsequent revision of this information.
|Phenotype Manifest In|
lea[robo2-8]/lea 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. lea[robo2-8]/lea[robo2-4] 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 lea[robo2-4]/lea[robo2-8] 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 lea[robo2-8]. The dendrite morphology of class I and class IV neurons is normal in lea[robo2-8] 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.
|Phenotype Manifest In|
lea[+]/learobo2-8, robo1 has presumptive embryonic/larval central nervous system phenotype, enhanceable by captk01217/capt[+]
|NOT Enhanced by|
learobo2-4/learobo2-8 has germline cell | embryonic stage phenotype, non-enhanceable by robo31/robo31
learobo2-4/learobo2-8 has gonadal sheath proper primordium | embryonic stage phenotype, non-enhanceable by robo31/robo31
|NOT Enhancer of|
learobo2-4/learobo2-8 is a non-enhancer of germline cell | embryonic stage phenotype of Df(2L)Exel7006/robo31
learobo2-4/learobo2-8 is a non-enhancer of gonad | embryonic stage phenotype of Df(2L)Exel7006/robo31
|NOT Suppressor of|
lea[+]/learobo2-8, robo1 has presumptive embryonic/larval central nervous system phenotype
lea[robo2-8]/+ fails to suppress the dorsal branch fusion phenotype seen when Sdc[dsRNA.Scer\UAS.cSa] is expressed under the control of Scer\GAL4[btl.PS].
Many of the dorsal abdominal clusters in robo/lea[robo2-8] 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 robo 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.
|Complementation & Rescue Data|
|Stocks ( 0 )|
|Notes on Origin|
|External Crossreferences & Linkouts|
|Synonyms & Secondary IDs ( 3 )|
(Kinrade and Hidalgo, 2004, Zhu et al., 2005, Lee et al., 2004, Johnson et al., 2004, Parsons et al., 2003, Wills et al., 2002, Englund et al., 2002, Dickson, 2001.3.14, Rajagopalan et al., 2000, Rajagopalan et al., 2000, Sano et al., 2005, Spitzweck et al., 2010, Dimitrova et al., 2008, Weyers et al., 2011, Schulz et al., 2011)
|Secondary FlyBase IDs|
|References ( 16 )|
|Personal communication to FlyBase|