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General Information
Symbol
Dmel\sli1
Species
D. melanogaster
Name
FlyBase ID
FBal0015699
Feature type
allele
Associated gene
Associated Insertion(s)
Carried in Construct
Also Known As
slit1
Allele class
Nature of the Allele
Allele class
Mutations Mapped to the Genome
 
Type
Location
Additional Notes
References
Associated Sequence Data
DNA sequence
Protein sequence
 
 
Progenitor genotype
Cytology
Nature of the lesion
Statement
Reference
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 )
 
Phenotypic Data
Phenotypic Class
Phenotype Manifest In
Detailed Description
Statement
Reference

Approximately 32% of heterozygous sli1 stage 16 embryos exhibit axon bundles that cross the midline incorrectly.

robo5,sli1/+,+ embryos typically display two to four axon bundles of the medial longitudinal pathway inappropriately crossing the midline per animal. The addition of enaGC1/+, enaGC5/+ or enaGC8/+ to these flies produces a dramatic enhancement of this phenotype, many more crossovers are seen, often several per segment. The addition of AblEP3101 driven by Scer\GAL4elav.PLu also enhances this phenotype, whilst the addition of Abl1 or Abl4 suppresses the phenotype.

All central nervous system axons converge on the midline in sli1/sli2 embryos.

embryonic lethal (homozygotes) Head involution abnormal. More severe abnormality in Df/sli than In the ventral nervous system, transverse commissures lacking entirely. Midline neurons and supportive mesectodermal cells missing. sli/sli indicates that sli is hypomorphic in nature.

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

robo15, sli1 has neuroanatomy defective phenotype, enhanceable by dock3

robo15, sli1 has neuroanatomy defective phenotype, enhanceable by Pak11

robo15, sli1 has neuroanatomy defective phenotype, enhanceable by Pak4

robo11, sli[+]/sli1 has neuroanatomy defective | dominant | embryonic stage 16 phenotype, enhanceable by Abl4/Abl[+]

NOT Enhanced by
Statement
Reference

robo[+]/robo15, sli1 has neuroanatomy defective phenotype, non-enhanceable by tutl[+]/tutlex383

robo15, sli[+]/sli1 has neuroanatomy defective phenotype, non-enhanceable by tutl[+]/tutlex383

Enhancer of
Statement
Reference

robo[+], sli[+], robo15, sli1 is an enhancer of neuroanatomy defective | embryonic stage 16 phenotype of kuze29-4

robo[+], sli[+], robo15, sli1 is an enhancer of neuroanatomy defective | embryonic stage 16 phenotype of kuzH143

sli[+]/sli1 is an enhancer of neuroanatomy defective | embryonic stage 16 phenotype of Abl4

Other
Phenotype Manifest In
Enhanced by
Statement
Reference

robo15, sli1 has MP1 neuron phenotype, enhanceable by dock04723

robo15, sli1 has pCC neuron phenotype, enhanceable by dock04723

robo15, sli1 has longitudinal connective phenotype, enhanceable by dock3

robo11, sli[+]/sli1 has longitudinal connective | embryonic stage 16 phenotype, enhanceable by Abl4/Abl[+]

sli1 has longitudinal connective phenotype, enhanceable by robo[+]/robo15

sli1 has longitudinal connective phenotype, enhanceable by robo[+]/ena[+]/enaGC1/robo15

sli1 has longitudinal connective phenotype, enhanceable by robo[+]/ena[+]/enaGC5/robo15

sli1 has longitudinal connective phenotype, enhanceable by robo[+]/ena[+]/enaGC8/robo15

robo15, sli[+]/sli1 has longitudinal connective phenotype, enhanceable by ena[+]/enaGC1

robo15, sli[+]/sli1 has longitudinal connective phenotype, enhanceable by ena[+]/enaGC5

robo15, sli[+]/sli1 has longitudinal connective phenotype, enhanceable by ena[+]/enaGC8

NOT Enhanced by
Statement
Reference
Suppressed by
Statement
Reference

sli1 has longitudinal connective phenotype, suppressible by robo[+]/Abl1/robo15/Abl[+]

sli1 has longitudinal connective phenotype, suppressible by robo[+]/Abl4/robo15/Abl[+]

robo15, sli[+]/sli1 has longitudinal connective phenotype, suppressible by Abl1/Abl[+]

robo15, sli[+]/sli1 has longitudinal connective phenotype, suppressible by Abl4/Abl[+]

Enhancer of
Statement
Reference
Other
Statement
Reference
Additional Comments
Genetic Interactions
Statement
Reference

sli[1], robo[5] transheterozygous stage 16 embryos exhibit thinner than normal fascicles and midline crossing defects.

A kuzH143 background enhances the FasII midline crossing phenotype seen in sli1, robo5 transheterozygous stage 16 embryos.

A kuze29-4 background enhances the FasII axon midline crossing phenotype seen in sli1, robo5 transheterozygous stage 16 embryos.

A kuz112 background enhances the FasII midline crossing phenotype seen in sli1, robo5 transheterozygous stage 16 embryos.

One copy each of sli1 and robo5 enhances the FasII axon midline crossing phenotype seen in kuzH143 stage 16 embryos.

Double heterozygous sli1/+, robo5/+ embryos exhibit minor defects in midline crossing.

In robo15/+, sli1/+ transheterozygous embryos, the medial longitudinal pathway occasionally crosses the midline. The addition of RhoGAP93BdsRNA.Scer\UAS (driven by Scer\GAL4elav.PLu) significantly enhances this phenotype.

When RhoGAP93BScer\UAS.cHa is driven by RhoGAP93BScer\UAS.cHa in a sli1/+, robo15/+ background, the axon scaffold of the ventral midline is severely disrupted. The ectopic crossing defect see at low frequency in sli1/+, robo15 embryos is enhanced.

In robo15/+, sli1/+ transheterozygous embryos, the medial longitudinal pathway occasionally crosses the midline. The addition of RacGAP84CScer\UAS.cRa (driven by Scer\GAL4elav.PLu) has no effect on this phenotype.

sli1, robo5 transheterozygotes exhibit approximately 2.7 defects in longitudinal axon guidance per animal. An average of 24% of segments show defects. Also 27% of embryos also exhibit defects in pCC/MP1. Heterozygous dock04723 enhances the longitudinal axon guidance and pCC/MP1 defects seen in transheterozygous sli1, robo5 mutants. An average of 7.4 defects are seen per animal. 67% of segments (calculated as number of defects/segments) show defects, and 72% of embryos show defects in pCC/MP1. Heterozygous dock3 enhances the longitudinal axon ectopic midline crossing defect seen in transheterozygous sli1, robo5 mutants. An average of 5.7 defects are seen per animal. 52% of segments (calculated as number of defects/segments) show defects. Overexpression of PakScer\UAS.T:Hsap\MYC under the control of Scer\GAL4elav.PLu enhances the longitudinal axon guidance and pCC/MP1 defects seen in transheterozygous sli1, robo5 mutants. An average of 6.1 defects are seen per animal. 55% of segments (calculated as number of defects/segments) show defects. Heterozygous Pak4 enhances the frequency of central nervous system axon defects seen in sli1, robo5 mutants. An average of 6.1 defects are seen per animal. 54% of segments (calculated as number of defects/segments) show defects. Heterozygous Pak11 enhances the frequency of central nervous system axon defects seen in sli1, robo5 mutants. An average of 5.8 defects are seen per animal. 53% of segments (calculated as number of defects/segments) show defects. Overexpression of PakScer\UAS.T:Myr1 under the control of Scer\GAL4elav.PLu enhances the longitudinal axon defects seen in transheterozygous sli1, robo5 mutants. An average of 14.3 defects are seen per animal. 130% of segments (calculated as number of defects/segments) show defects.

sli1, robo5 transheterozygotes exhibit approximately 2.7 defects in longitudinal axon guidance per animal. An average of 24% of segments show defects. Also 27% of embryos also exhibit defects in pCC/MP1.

Heterozygous dock04723 enhances the longitudinal axon guidance and pCC/MP1 defects seen in transheterozygous sli1, robo5 mutants. An average of 7.4 defects are seen per animal. 67% of segments (calculated as number of defects/segments) show defects, and 72% of embryos show defects in pCC/MP1.

Heterozygous dock3 enhances the longitudinal axon ectopic midline crossing defect seen in transheterozygous sli1, robo5 mutants. An average of 5.7 defects are seen per animal. 52% of segments (calculated as number of defects/segments) show defects.

Overexpression of PakScer\UAS.T:Hsap\MYC under the control of Scer\GAL4elav.PLu enhances the longitudinal axon guidance and pCC/MP1 defects seen in transheterozygous sli1, robo5 mutants. An average of 6.1 defects are seen per animal. 55% of segments (calculated as number of defects/segments) show defects.

Heterozygous Pak4 enhances the frequency of central nervous system axon defects seen in sli1, robo5 mutants. An average of 6.1 defects are seen per animal. 54% of segments (calculated as number of defects/segments) show defects.

Heterozygous Pak11 enhances the frequency of central nervous system axon defects seen in sli1, robo5 mutants. An average of 5.8 defects are seen per animal. 53% of segments (calculated as number of defects/segments) show defects.

Overexpression of PakScer\UAS.T:Myr1 under the control of Scer\GAL4elav.PLu enhances the longitudinal axon defects seen in transheterozygous sli1, robo5 mutants. An average of 14.3 defects are seen per animal.

A few axon bundles cross the midline incorrectly in embryos trans-heterozygous for robo1 and sli1. This combination increases the penetrance of crossovers to about 60%.

When one copy of Abl4 is also present in trans-heterozygous robo1 and sli1 embryos, several abnormal crossovers are observed in all embryos examined, and some axon bundles collapse towards the midline in a manner reminiscent of a sli1 phenotype.

Heterozygous sli1 enhances the number of abnormal axon crossovers observed in Abl4 mutants.

The addition of one mutant copy of Abl4 doubles the number of crossovers observed in heterozygous sli1 mutants.

Compared with heterozygous sli1 mutants alone, pan-neural overexpression of AblScer\UAS.cHa using Scer\GAL4elav.PLu enhances the frequency of abnormal axonal crossovers. Scer\GAL4elav.PLu>AblScer\UAS.cHa expression causes axons to cross the midline inappropriately in most segments of all embryos in sli1 heterozygous mutants.

In sli1/+,robo5/+ double heterozygote embryos the occasional axon crosses the midline. This phenotype is dramatically enhanced by Nedd4Scer\UAS.T:Hsap\MYC.

Over half of sim2, sli1 embryos exhibit a 'collapsed axon' phenotype, about a third a have fused commissures. Midline cells are displaced ventrally in these embryos. Half of jing01094, sli1 double homozygous embryos exhibit a 'collapsed axon' phenotype, about a third a have fused commissures. Midline cells are displaced ventrally in these embryos.

28% of segments contain Fas2-positive neurons inappropriately crossing the midline in sli1/robo1 double heterozygous embryos, in contrast to either single heterozygote which do not show this defect. 26% of segments contain Fas2-positive neurons inappropriately crossing the midline in sli1/robo4 double heterozygous embryos, in contrast to either single heterozygote which show defects in 0 or 1% of segments. sli1 dominantly enhances the robo5 phenotype, resulting in a lateral compression of the axon scaffold in the central nervous system. sli1 robo5 double homozygotes have a phenotype similar to that of sli1 single homozygotes.

Xenogenetic Interactions
Statement
Reference

Pan-neural expression of Abl::Hsap\ABL1::Hsap\BCRP210.Scer\UAS in heterozygous sli1 mutants results in a collapse of the longitudinal connectives towards the midline.

Expression of Abl::Hsap\ABL1::Hsap\BCRKR.Scer\UAS using Scer\GAL4elav.PLu enhances the midline-crossing phenotype of axon bundles in heterozygous sli1 embryos.

Complementation and Rescue Data
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Synonyms and Secondary IDs (4)
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    References (12)