Allele Dmel\sli¹

General Information
Symbol	Dmel\sli¹	Species	D. melanogaster
Name		FlyBase ID	FBal0015699
Feature type	allele	Associated gene	Dmel\sli
Also Known As	slit¹

Allele class
Mutagen	ethyl methanesulfonate
Recent Updates
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FB2013_03
FB2013_02
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Nature of the Allele
Allele class
Mutagen	ethyl methanesulfonate (Tearle and Nusslein-Volhard, 1987)
Mutations Mapped to the Genome

Type Location Additional Notes References
Associated Sequence Data
DDBJ / EMBL / GenBank	DNA sequence Protein sequence Name

UniProtKB/Swiss-Prot
UniProtKB/TrEMBL

Progenitor genotype
Nature of the lesion	Statement Reference
Cytology
Phenotypic Data
Phenotypic Class

Phenotype Manifest In
	presumptive embryonic/larval central nervous system (Sun et al., 2000)
Detailed Description
	Statement Reference robo⁵,sli¹/+,+ embryos typically display two to four axon bundles of the medial longitudinal pathway inappropriately crossing the midline per animal. The addition of ena^GC1/+, ena^GC5/+ or ena^GC8/+ to these flies produces a dramatic enhancement of this phenotype, many more crossovers are seen, often several per segment. The addition of Abl^EP3101 driven by Scer\GAL4^elav.PLu also enhances this phenotype, whilst the addition of Abl¹ or Abl⁴ suppresses the phenotype. (Bashaw et al., 2000) All central nervous system axons converge on the midline in sli¹/sli² embryos. (Sun et al., 2000) 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
Linkouts
Interactions
	Show the genetic interaction network for Enhancers & Suppressors
Phenotypic Class
Enhanced by
Statement Reference robo[+]/robo⁵, sli¹ has neuroanatomy defective \| dominant phenotype, enhanceable by Scer\GAL4^elav-C155/Nedd4^{Scer\UAS.T:Hsap\MYC}, robo[+]/robo⁵ (Myat et al., 2002) robo⁵, sli[+]/sli¹ has neuroanatomy defective \| dominant \| embryonic stage 16 phenotype, enhanceable by kuz¹¹² (Coleman et al., 2010) robo⁵, sli[+]/sli¹ has neuroanatomy defective \| dominant \| embryonic stage 16 phenotype, enhanceable by kuz^e29-4 (Coleman et al., 2010) robo⁵, sli[+]/sli¹ has neuroanatomy defective \| dominant \| embryonic stage 16 phenotype, enhanceable by kuz^H143 (Coleman et al., 2010) robo⁵, sli[+]/sli¹ has neuroanatomy defective \| dominant phenotype, enhanceable by Scer\GAL4^elav-C155/Nedd4^{Scer\UAS.T:Hsap\MYC} (Myat et al., 2002) robo⁵, sli¹ has neuroanatomy defective phenotype, enhanceable by dock³ (Fan et al., 2003) robo⁵, sli¹ has neuroanatomy defective phenotype, enhanceable by dock⁰⁴⁷²³ (Fan et al., 2003) robo⁵, sli¹ has neuroanatomy defective phenotype, enhanceable by Pak⁴ (Fan et al., 2003) robo⁵, sli¹ has neuroanatomy defective phenotype, enhanceable by Pak¹¹ (Fan et al., 2003) robo⁵, sli¹ has neuroanatomy defective phenotype, enhanceable by Pak^{Scer\UAS.T:Hsap\MYC}/Scer\GAL4^elav.PLu (Fan et al., 2003) robo⁵, sli¹ has neuroanatomy defective phenotype, enhanceable by Scer\GAL4^elav.PLu/Pak^{Scer\UAS.T:Myr-Src64B} (Fan et al., 2003)
NOT Enhanced by
Statement Reference robo[+]/robo⁵, sli¹ has neuroanatomy defective phenotype, non-enhanceable by tutl[+]/tutl^ex383 (Al-Anzi and Wyman, 2009) robo⁵, sli[+]/sli¹ has neuroanatomy defective phenotype, non-enhanceable by tutl[+]/tutl^ex383 (Al-Anzi and Wyman, 2009)
Enhancer of
Statement Reference robo[+], sli[+], robo⁵, sli¹ is an enhancer of neuroanatomy defective \| embryonic stage 16 phenotype of kuz^e29-4 (Coleman et al., 2010) robo[+], sli[+], robo⁵, sli¹ is an enhancer of neuroanatomy defective \| embryonic stage 16 phenotype of kuz^H143 (Coleman et al., 2010)
Other
Statement Reference robo[+]/robo⁵, sli¹ has neuroanatomy defective \| dominant phenotype (Myat et al., 2002) robo[+]/robo⁵, sli¹ has neuroanatomy defective phenotype (Al-Anzi and Wyman, 2009) robo⁵, sli[+]/sli¹ has neuroanatomy defective \| dominant \| embryonic stage 16 phenotype (Coleman et al., 2010) robo⁵, sli[+]/sli¹ has neuroanatomy defective \| dominant phenotype (Myat et al., 2002) robo⁵, sli[+]/sli¹ has neuroanatomy defective phenotype (Al-Anzi and Wyman, 2009) robo⁵, sli¹ has neuroanatomy defective \| dominant phenotype (Myat et al., 2002, Myat et al., 2002) robo⁵, sli¹ has neuroanatomy defective phenotype (Fan et al., 2003, Fan et al., 2003)
Phenotype Manifest In
Enhanced by
Statement Reference robo[+]/robo⁵, sli¹ has anterior commissure phenotype, enhanceable by Scer\GAL4^elav-C155/Nedd4^{Scer\UAS.T:Hsap\MYC}, robo[+]/robo⁵ (Myat et al., 2002) robo[+]/robo⁵, sli¹ has posterior commissure phenotype, enhanceable by Scer\GAL4^elav-C155/Nedd4^{Scer\UAS.T:Hsap\MYC}, robo[+]/robo⁵ (Myat et al., 2002) robo[+]/robo⁵, sli¹ has ventral nerve cord phenotype, enhanceable by Scer\GAL4^elav-C155/Nedd4^{Scer\UAS.T:Hsap\MYC}, robo[+]/robo⁵ (Myat et al., 2002) robo⁵, sli[+]/sli¹ has anterior commissure phenotype, enhanceable by Scer\GAL4^elav-C155/Nedd4^{Scer\UAS.T:Hsap\MYC} (Myat et al., 2002) robo⁵, sli[+]/sli¹ has longitudinal connective \| embryonic stage 16 phenotype, enhanceable by kuz¹¹² (Coleman et al., 2010) robo⁵, sli[+]/sli¹ has longitudinal connective \| embryonic stage 16 phenotype, enhanceable by kuz^e29-4 (Coleman et al., 2010) robo⁵, sli[+]/sli¹ has longitudinal connective \| embryonic stage 16 phenotype, enhanceable by kuz^H143 (Coleman et al., 2010) robo⁵, sli[+]/sli¹ has longitudinal connective phenotype, enhanceable by Abl^EP3101/Scer\GAL4^elav.PLu (Bashaw et al., 2000) robo⁵, sli[+]/sli¹ has longitudinal connective phenotype, enhanceable by ena[+]/ena^GC1 (Bashaw et al., 2000) robo⁵, sli[+]/sli¹ has longitudinal connective phenotype, enhanceable by ena[+]/ena^GC5 (Bashaw et al., 2000) robo⁵, sli[+]/sli¹ has longitudinal connective phenotype, enhanceable by ena[+]/ena^GC8 (Bashaw et al., 2000) robo⁵, sli[+]/sli¹ has midline crossing tract \| embryonic stage 16 phenotype, enhanceable by kuz¹¹² (Coleman et al., 2010) robo⁵, sli[+]/sli¹ has midline crossing tract \| embryonic stage 16 phenotype, enhanceable by kuz^e29-4 (Coleman et al., 2010) robo⁵, sli[+]/sli¹ has midline crossing tract \| embryonic stage 16 phenotype, enhanceable by kuz^H143 (Coleman et al., 2010) robo⁵, sli[+]/sli¹ has posterior commissure phenotype, enhanceable by Scer\GAL4^elav-C155/Nedd4^{Scer\UAS.T:Hsap\MYC} (Myat et al., 2002) robo⁵, sli[+]/sli¹ has ventral nerve cord phenotype, enhanceable by Scer\GAL4^elav-C155/Nedd4^{Scer\UAS.T:Hsap\MYC} (Myat et al., 2002) robo⁵, sli¹ has longitudinal connective phenotype, enhanceable by dock³ (Fan et al., 2003) robo⁵, sli¹ has longitudinal connective phenotype, enhanceable by dock⁰⁴⁷²³ (Fan et al., 2003) robo⁵, sli¹ has longitudinal connective phenotype, enhanceable by Pak^{Scer\UAS.T:Hsap\MYC}/Scer\GAL4^elav.PLu (Fan et al., 2003) robo⁵, sli¹ has longitudinal connective phenotype, enhanceable by Scer\GAL4^elav.PLu/Pak^{Scer\UAS.T:Myr-Src64B} (Fan et al., 2003) robo⁵, sli¹ has medial longitudinal fascicle phenotype, enhanceable by RhoGAP93B^{dsRNA.Scer\UAS}/Scer\GAL4^elav.PLu (Hu et al., 2005) robo⁵, sli¹ has MP1 neuron phenotype, enhanceable by dock⁰⁴⁷²³ (Fan et al., 2003) robo⁵, sli¹ has pCC neuron phenotype, enhanceable by dock⁰⁴⁷²³ (Fan et al., 2003) sli¹ has longitudinal connective phenotype, enhanceable by Abl^EP3101/robo⁵/Scer\GAL4^elav.PLu (Bashaw et al., 2000) sli¹ has longitudinal connective phenotype, enhanceable by robo[+]/ena[+]/ena^GC1/robo⁵ (Bashaw et al., 2000) sli¹ has longitudinal connective phenotype, enhanceable by robo[+]/ena[+]/ena^GC5/robo⁵ (Bashaw et al., 2000) sli¹ has longitudinal connective phenotype, enhanceable by robo[+]/ena[+]/ena^GC8/robo⁵ (Bashaw et al., 2000) sli¹ has longitudinal connective phenotype, enhanceable by robo[+]/robo⁵ (Bashaw et al., 2000)
NOT Enhanced by
Statement Reference robo[+]/robo⁵, sli¹ has midline crossing tract phenotype, non-enhanceable by tutl[+]/tutl^ex383 (Al-Anzi and Wyman, 2009) robo⁵, sli[+]/sli¹ has midline crossing tract phenotype, non-enhanceable by tutl[+]/tutl^ex383 (Al-Anzi and Wyman, 2009) robo⁵, sli¹ has medial longitudinal fascicle phenotype, non-enhanceable by CdGAPr^{dsRNA.H.Scer\UAS}/Scer\GAL4^elav.PLu (Hu et al., 2005) robo⁵, sli¹ has medial longitudinal fascicle phenotype, non-enhanceable by RacGAP84C^Scer\UAS.cRa/Scer\GAL4^elav.PLu (Hu et al., 2005) robo⁵, sli¹ has medial longitudinal fascicle phenotype, non-enhanceable by RhoGAP19D^{dsRNA.H.Scer\UAS}/Scer\GAL4^elav.PLu (Hu et al., 2005) robo⁵, sli¹ has medial longitudinal fascicle phenotype, non-enhanceable by RhoGAP100F^{dsRNA.H.Scer\UAS}/Scer\GAL4^elav.PLu (Hu et al., 2005) robo⁵, sli¹ has medial longitudinal fascicle phenotype, non-enhanceable by RhoGAPp190^{dsRNA.Scer\UAS}/Scer\GAL4^elav.PLu (Hu et al., 2005) robo⁵, sli¹ has medial longitudinal fascicle phenotype, non-enhanceable by tum^{dsRNA.H.Scer\UAS}/Scer\GAL4^elav.PLu (Hu et al., 2005)
Suppressed by
Statement Reference robo⁵, sli[+]/sli¹ has longitudinal connective phenotype, suppressible by Abl¹/Abl[+] (Bashaw et al., 2000) robo⁵, sli[+]/sli¹ has longitudinal connective phenotype, suppressible by Abl⁴/Abl[+] (Bashaw et al., 2000) sli¹ has longitudinal connective phenotype, suppressible by robo[+]/Abl¹/robo⁵/Abl[+] (Bashaw et al., 2000) sli¹ has longitudinal connective phenotype, suppressible by robo[+]/Abl⁴/robo⁵/Abl[+] (Bashaw et al., 2000)
Enhancer of
Statement Reference robo[+], sli[+], robo⁵, sli¹ is an enhancer of longitudinal connective \| embryonic stage 16 phenotype of kuz^e29-4 (Coleman et al., 2010) robo[+], sli[+], robo⁵, sli¹ is an enhancer of longitudinal connective \| embryonic stage 16 phenotype of kuz^H143 (Coleman et al., 2010) robo[+], sli[+], robo⁵, sli¹ is an enhancer of midline crossing tract \| embryonic stage 16 phenotype of kuz^e29-4 (Coleman et al., 2010) robo[+], sli[+], robo⁵, sli¹ is an enhancer of midline crossing tract \| embryonic stage 16 phenotype of kuz^H143 (Coleman et al., 2010) sli[+]/sli¹ is an enhancer of longitudinal connective phenotype of sim² (Sedaghat et al., 2002) sli[+]/sli¹ is an enhancer of presumptive embryonic/larval central nervous system phenotype of jing⁰¹⁰⁹⁴ (Sedaghat et al., 2002) sli[+]/sli¹ is an enhancer of presumptive embryonic/larval central nervous system phenotype of sim² (Sedaghat et al., 2002) sli¹ is an enhancer of longitudinal connective phenotype of robo⁵ (Bashaw et al., 2000) sli¹ is an enhancer of presumptive embryonic/larval central nervous system phenotype of robo⁵ (Kidd et al., 1999)
Other
Statement Reference jing[+]/jing⁰¹⁰⁹⁴, sli¹ has presumptive embryonic/larval central nervous system phenotype (Sedaghat et al., 2002) jing[+]/jing⁰¹⁰⁹⁴, sli¹ has ventral midline phenotype (Sedaghat et al., 2002) jing⁰¹⁰⁹⁴, sli[+]/sli¹ has ventral midline phenotype (Sedaghat et al., 2002) jing⁰¹⁰⁹⁴, sli¹ has presumptive embryonic/larval central nervous system phenotype (Sedaghat et al., 2002) jing⁰¹⁰⁹⁴, sli¹ has ventral midline phenotype (Sedaghat et al., 2002, Sedaghat et al., 2002) robo[+]/robo⁵, sli¹ has anterior commissure phenotype (Myat et al., 2002) robo[+]/robo⁵, sli¹ has midline crossing tract phenotype (Al-Anzi and Wyman, 2009) robo[+]/robo⁵, sli¹ has posterior commissure phenotype (Myat et al., 2002) robo[+]/robo⁵, sli¹ has ventral nerve cord phenotype (Myat et al., 2002) robo¹, sli¹ has presumptive embryonic/larval central nervous system phenotype (Kidd et al., 1999, Kidd et al., 1999) robo⁴, sli¹ has presumptive embryonic/larval central nervous system phenotype (Kidd et al., 1999, Kidd et al., 1999) robo⁵, sli[+]/sli¹ has anterior commissure phenotype (Myat et al., 2002) robo⁵, sli[+]/sli¹ has longitudinal connective \| embryonic stage 16 phenotype (Coleman et al., 2010) robo⁵, sli[+]/sli¹ has midline crossing tract \| embryonic stage 16 phenotype (Coleman et al., 2010) robo⁵, sli[+]/sli¹ has midline crossing tract phenotype (Al-Anzi and Wyman, 2009) robo⁵, sli[+]/sli¹ has posterior commissure phenotype (Myat et al., 2002) robo⁵, sli¹ has anterior commissure phenotype (Myat et al., 2002, Myat et al., 2002) robo⁵, sli¹ has longitudinal connective phenotype (Fan et al., 2003, Fan et al., 2003) robo⁵, sli¹ has medial longitudinal fascicle phenotype (Hu et al., 2005, Hu et al., 2005) robo⁵, sli¹ has MP1 neuron phenotype (Fan et al., 2003, Fan et al., 2003) robo⁵, sli¹ has pCC neuron phenotype (Fan et al., 2003, Fan et al., 2003) robo⁵, sli¹ has posterior commissure phenotype (Myat et al., 2002, Myat et al., 2002) robo⁵, sli¹ has ventral nerve cord phenotype (Myat et al., 2002, Myat et al., 2002) sim², sli[+]/sli¹ has ventral midline phenotype (Sedaghat et al., 2002) sim², sli¹ has presumptive embryonic/larval central nervous system phenotype (Sedaghat et al., 2002) sim², sli¹ has ventral midline phenotype (Sedaghat et al., 2002, Sedaghat et al., 2002) sim²/sim[+], sli¹ has presumptive embryonic/larval central nervous system phenotype (Sedaghat et al., 2002) sim²/sim[+], sli¹ has ventral midline phenotype (Sedaghat et al., 2002)
Additional Comments
Genetic Interactions
Statement Reference sli[1], robo[5] transheterozygous stage 16 embryos exhibit thinner than normal fascicles and midline crossing defects. A kuz[H143] background enhances the FasII midline crossing phenotype seen in sli[1], robo[5] transheterozygous stage 16 embryos. A kuz[e29-4] background enhances the FasII axon midline crossing phenotype seen in sli[1], robo[5] transheterozygous stage 16 embryos. A kuz[112] background enhances the FasII midline crossing phenotype seen in sli[1], robo[5] transheterozygous stage 16 embryos. One copy each of sli[1] and robo[5] enhances the FasII axon midline crossing phenotype seen in kuz[H143] stage 16 embryos. (Coleman et al., 2010) Double heterozygous sli[1]/+, robo[5]/+ embryos exhibit minor defects in midline crossing. (Al-Anzi and Wyman, 2009) In robo⁵/+, sli¹/+ transheterozygous embryos, the medial longitudinal pathway occasionally crosses the midline. The addition of RhoGAP93B^{dsRNA.Scer\UAS} (driven by Scer\GAL4^elav.PLu) significantly enhances this phenotype. The subsequent addition of RhoGAP93B^Scer\UAS.cHa suppresses this enhancement. In robo⁵/+, sli¹/+ transheterozygous embryos, the medial longitudinal pathway occasionally crosses the midline. The addition of RhoGAPp190^{dsRNA.Scer\UAS}, RhoGAP19D^{dsRNA.H.Scer\UAS}, CdGAPr^{dsRNA.H.Scer\UAS}, RacGAP50C^{dsRNA.H.Scer\UAS}, RhoGAP100F^{dsRNA.H.Scer\UAS} (driven by Scer\GAL4^elav.PLu) does not enhance this phenotype. In robo⁵/+, sli¹/+ transheterozygous embryos, the medial longitudinal pathway occasionally crosses the midline. The addition of RacGAP84C^Scer\UAS.cRa (driven by Scer\GAL4^elav.PLu) has no effect on this phenotype. (Hu et al., 2005) 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 Pak^{Scer\UAS.T:Hsap\MYC} under the control of Scer\GAL4^elav.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 Pak^{Scer\UAS.T:Myr1} under the control of Scer\GAL4^elav.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. (Fan et al., 2003) 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 Pak^{Scer\UAS.T:Hsap\MYC} under the control of Scer\GAL4^elav.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 Pak^{Scer\UAS.T:Myr1} under the control of Scer\GAL4^elav.PLu enhances the longitudinal axon defects seen in transheterozygous sli¹, robo⁵ mutants. An average of 14.3 defects are seen per animal. (Fan et al., 2003) In sli¹/+,robo⁵/+ double heterozygote embryos the occasional axon crosses the midline. This phenotype is dramatically enhanced by Nedd4^{Scer\UAS.T:Hsap\MYC}. (Myat et al., 2002) 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. (Sedaghat et al., 2002) 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. (Kidd et al., 1999)
Xenogenetic Interactions
Statement Reference
Complementation & Rescue Data
Comments
Stocks ( 0 )

Notes on Origin
Discoverer

External Crossreferences & Linkouts
Other Crossreferences

Linkouts

Synonyms & Secondary IDs ( 4 )
Reported As
Symbol Synonym	sli¹ (Fan et al., 2003) sli^IG2 (Tearle and Nusslein-Volhard, 1987, ) sli^IG3 slit¹ (Myat et al., 2002, Al-Anzi and Wyman, 2009, Coleman et al., 2010)
Name Synonym
Secondary FlyBase IDs

References ( 11 )
Research paper	Coleman et al., 2010, Development 137(14): 2417--2426 The Adam family metalloprotease Kuzbanian regulates the cleavage of the roundabout receptor to control axon repulsion at the midline. [FBrf0211121] Al-Anzi and Wyman, 2009, Neural Dev. 4: 31 The Drosophila immunoglobulin gene turtle encodes guidance molecules involved in axon pathfinding. [FBrf0209104] Hu et al., 2005, Proc. Natl. Acad. Sci. U.S.A. 102(12): 4613--4618 Cross GTPase-activating protein (CrossGAP)/Vilse links the Roundabout receptor to Rac to regulate midline repulsion. [FBrf0191476] Fan et al., 2003, Neuron 40(1): 113--127 Slit stimulation recruits Dock and Pak to the roundabout receptor and increases Rac activity to regulate axon repulsion at the CNS midline. [FBrf0167957] Myat et al., 2002, Neuron 35(3): 447--459 Drosophila nedd4, a ubiquitin ligase, is recruited by commissureless to control cell surface levels of the roundabout receptor. [FBrf0151451] Sedaghat et al., 2002, Development 129(11): 2591--2606 The jing Zn-finger transcription factor is a mediator of cellular differentiation in the Drosophila CNS midline and trachea. [FBrf0148962] Bashaw et al., 2000, Cell 101(7): 703--715 Repulsive axon guidance: abelson and enabled play opposing roles downstream of the roundabout receptor. [FBrf0128391] Simpson et al., 2000, Neuron 28(3): 753--766 Short-range and long-range guidance by Slit and its Robo receptors: robo and Robo2 play distinct roles in midline guidance. [FBrf0132431] Sun et al., 2000, Development 127(4): 801--812 Receptor tyrosine phosphatases regulate axon guidance across the midline of the Drosophila embryo. [FBrf0125454] Kidd et al., 1999, Cell 96(6): 785--794 Slit is the midline repellent for the robo receptor in Drosophila. [FBrf0107807]
Stock list	Tearle and Nusslein-Volhard, 1987, D. I. S. 66: 209--269 Tubingen mutants and stock list. [FBrf0045941]

Allele Dmel\sli1

Allele Dmel\sli¹