FlyBase Allele Report: Dmel\robo2[x135]

General Information

Symbol

Dmel\robo2^x135

Species

D. melanogaster

Name

FlyBase ID

FBal0147046

Feature type

allele

Associated gene

Dmel\robo2

Associated Insertion(s)

Carried in Construct

Key Links

Allele class

Mutagen

Nature of the Allele

Allele class

Mutagen

Progenitor genotype

P{EP}robo2^EP2582

(Simpson et al., 2000)

Cytology

Description

Deletions of 1-2 kb that removes the first exon of lea, which includes the translation site and the signal sequence.

(Simpson et al., 2000)

Mutations Mapped to the Genome

Curation Data

Type

Location

Additional Notes

References

Variant Molecular Consequences

Associated Sequence Data

DDBJ / EMBL / GenBank

DNA sequence

Protein sequence

UniProtKB/Swiss-Prot

UniProtKB/TrEMBL

Expression Data

Reporter Expression

Additional Information

Statement

Reference

Marker for

Reflects expression of

Reporter construct used in assay

Human Disease Associations

Disease Ontology (DO) Annotations

Models Based on Experimental Evidence ( 0 )

Disease

Evidence

References

Modifiers Based on Experimental Evidence ( 0 )

Disease

Interaction

References

Comments on Models/Modifiers Based on Experimental Evidence ( 0 )

Disease-implicated variant(s)

Phenotypic Data

Phenotypic Class

abnormal neuroanatomy

(Parsons et al., 2003)

abnormal neuroanatomy | embryonic stage (with robo2^X123)

(Howard et al., 2021)

Phenotype Manifest In

Detailed Description

Statement

Reference

robo2^X123/robo2^x135 embryos have a mildly disorganised acon scaffold in the central nervous system, but do not show defects in crossing of the midline by EW neurons.

(Evans et al., 2015)

Mutant embryos do not show transformation of the thoracic dch3 chordotonal organs to a morphology resembling that of abdominal lch5 chordotonal organs.

(Kraut and Zinn, 2004)

The lch5 axons are stalled, most frequently before turning point TP1 but sometimes between turning points TP1 and TP2, in 3% 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. The abnormally projecting axons can project anteriorly, posteriorly or dorsally. The anteriorly or posteriorly projecting axons sometimes rejoin the intersegmental nerve further ventrally. The abnormal trajectories start from the level of the neuron cell bodies, suggesting that the trajectory defects arise from early stages of axon outgrowth. In some cases the entire dorsal cluster fascicle projects in an abnormal direction, while in other cases only a subset of axons is affected. The morphology of the dorsal trunk, transverse connective and dorsal branches is usually normal. The morphology of the tracheal system is normal in hemisegments in which abnormal dorsal axon morphologies occur.

(Parsons et al., 2003)

The ch neuron projections in embryos are generally unaffected. The dbd neuron projection is unchanged.

(Zlatic et al., 2003)

Fas2 staining axons in the central nervous system (CNS) exhibit clear mutant phenotypes. Some axons ectopically cross the midline. There is also disorganisation of the longitudinal tracts. This appears as "braiding". Instead of maintaining their parallel alignment the three Fas2 bundles on each side of the CNS cross over and intermittently join with each other on their own side. Segments that show misrouting of axons between bundles on the same side are more common that those that show axons crossing the midline. Con staining axons are often fused into a single group of axons. The overexpression of lea^Scer\UAS.cSa in all neurons in a lea^x135 background causes much more severe disruptions in axon pathfinding than in lea^x135 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 lea^Scer\UAS.cSa overexpression in a wild-type background.

(Simpson et al., 2000)

External Data

Linkouts

Interactions

Show genetic interaction network for Enhancers & Suppressors

Phenotypic Class

Enhancer of

Statement

Reference

robo2^X123/robo2^x135 is an enhancer of abnormal neuroanatomy phenotype of fra³/fra⁴

(Evans et al., 2015)

Phenotype Manifest In

Enhanced by

Statement

Reference

robo2^x135 has presumptive embryonic/larval central nervous system phenotype, enhanceable by robo[+]/robo1^unspecified

(Simpson et al., 2000)

robo2^x135 has larval longitudinal connective phenotype, enhanceable by robo[+]/robo1^unspecified

(Simpson et al., 2000)

robo2^x135 has larval ventral nerve cord phenotype, enhanceable by robo[+]/robo1^unspecified

(Simpson et al., 2000)

robo2^x135 has presumptive embryonic/larval central nervous system phenotype, enhanceable by robo1^unspecified/robo1^unspecified

(Simpson et al., 2000)

robo2^x135 has larval longitudinal connective phenotype, enhanceable by robo1^unspecified/robo1^unspecified

(Simpson et al., 2000)

robo2^x135 has larval ventral nerve cord phenotype, enhanceable by robo1^unspecified/robo1^unspecified

(Simpson et al., 2000)

Enhancer of

Statement

Reference

robo2^X123/robo2^x135 is an enhancer of symmetrical commissure phenotype of fra³/fra⁴

(Evans et al., 2015)

robo2^X123/robo2^x135 is an enhancer of larval EW neuron phenotype of fra³/fra⁴

(Evans et al., 2015)

Other

Statement

Reference

robo1¹, robo2^x135 has metathoracic dorsal triscolopidial chordotonal organ dch3 phenotype

(Kraut and Zinn, 2004)

robo1¹, robo2^x135 has mesothoracic dorsal triscolopidial chordotonal organ dch3 phenotype

(Kraut and Zinn, 2004)

Additional Comments

Genetic Interactions

Statement

Reference

35.9% of thoracic segments show transformation of the dch3 chordotonal organs to a morphology resembling that of abdominal lch5 chordotonal organs in robo¹ lea^x135 double mutant embryos. 11.2% of thoracic segments show transformation of the dch3 chordotonal organs to a morphology resembling that of abdominal lch5 chordotonal organs in robo⁷ lea^x135 double mutant embryos that are expressing lea^{Scer\UAS.T:Hsap\MYC} under the control of Scer\GAL4^elav-C155. 16% of thoracic segments show transformation of the dch3 chordotonal organs to a morphology resembling that of abdominal lch5 chordotonal organs in robo⁷ lea^x135 double mutant embryos that are expressing lea^{Scer\UAS.T:Hsap\MYC} under the control of Scer\GAL4^48Y.

(Kraut and Zinn, 2004)

Embryos homozygous mutant for robo^unspecified and lea^x135 show a compressed midline where all the axons approach the midline and cannot leave. The addition of comm^Δe39 does not effect this phenotype. Embryos heterozygous for lea^x135/+ and homozygous robo^unspecified, show ectopic crossing of the medial Fas2 pathway but the medial pathway collapses entirely onto the midline. Embryos heterozygous for robo^unspecified/+ and homozygous lea^x135 much more ectopic crossing is seen than in lea^x135 homozygotes.

(Simpson et al., 2000)

Xenogenetic Interactions

Statement

Reference

Complementation and Rescue Data

Not rescued by

robo2^x135 is not rescued by Scer\GAL4^tracheal/robo2^{UAS.Tag:HA,Tag:SS(wg)}

(Parsons et al., 2003)

robo2^x135 is not rescued by Scer\GAL4^elav-C155/robo2^{UAS.Tag:HA,Tag:SS(wg)}

(Parsons et al., 2003)

Comments

Images (0)

Mutant

Wild-type

Stocks (0)

Notes on Origin

Discoverer

Described in FBrf0132431.

(Zlatic et al., 2003)

External Crossreferences and Linkouts ( 0 )

Synonyms and Secondary IDs (5)

Reported As

Symbol Synonym

lea^x135

robo2¹³⁵

(Howard et al., 2021)

robo2^X135

(Parsons et al., 2003)

robo2^ex135

(Kraut and Zinn, 2004)

robo2^x135

(Gonsior and Ismat, 2019, Santiago and Bashaw, 2017, Evans et al., 2015, Zlatic et al., 2003)

Name Synonyms

Secondary FlyBase IDs

References (9)

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