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.
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.
robo15, sli[+]/sli1 has abnormal neuroanatomy | embryonic stage 16 | dominant phenotype, enhanceable by kuzH143
robo15, sli[+]/sli1 has abnormal neuroanatomy | embryonic stage 16 | dominant phenotype, enhanceable by kuz112
robo15, sli[+]/sli1 has abnormal neuroanatomy | embryonic stage 16 | dominant phenotype, enhanceable by kuze29-4
robo15, sli1 has abnormal neuroanatomy phenotype, enhanceable by dock04723
robo15, sli1 has abnormal neuroanatomy phenotype, enhanceable by dock3
robo15, sli1 has abnormal neuroanatomy phenotype, enhanceable by Pak11
robo15, sli1 has abnormal neuroanatomy phenotype, enhanceable by Pak4
robo15, sli1 has abnormal neuroanatomy phenotype, enhanceable by PakUAS.Tag:MYC/Scer\GAL4elav.PLu
robo15, sli1 has abnormal neuroanatomy phenotype, enhanceable by Scer\GAL4elav.PLu/PakUAS.Tag:Myr(Src64B)
robo11, sli[+]/sli1 has abnormal neuroanatomy | embryonic stage 16 | dominant phenotype, enhanceable by Abl4/Abl[+]
sli1 has abnormal neuroanatomy | embryonic stage 16 | dominant phenotype, enhanceable by Abl4/Abl[+]
sli1 has abnormal neuroanatomy | embryonic stage 16 | dominant phenotype, enhanceable by AblUAS.cHa/Scer\GAL4elav.PLu
sli1 has abnormal neuroanatomy | embryonic stage 16 | dominant phenotype, enhanceable by Scer\GAL4elav.PLu/Abl::Hsap\ABL1::Hsap\BCRP210.UAS
sli1 has abnormal neuroanatomy | embryonic stage 16 | dominant phenotype, enhanceable by Abl::Hsap\ABL1::Hsap\BCRKR.UAS/Scer\GAL4elav.PLu
robo15, sli[+]/sli1 has abnormal neuroanatomy | dominant phenotype, enhanceable by Scer\GAL4elav-C155/Nedd4UAS.Tag:MYC
robo[+]/robo15, sli1 has abnormal neuroanatomy phenotype, non-enhanceable by tutl[+]/tutlex383
robo15, sli[+]/sli1 has abnormal neuroanatomy phenotype, non-enhanceable by tutl[+]/tutlex383
robo[+], sli[+], robo15, sli1 is an enhancer of abnormal neuroanatomy | embryonic stage 16 phenotype of kuze29-4
robo[+], sli[+], robo15, sli1 is an enhancer of abnormal neuroanatomy | embryonic stage 16 phenotype of kuzH143
sli[+]/sli1 is an enhancer of abnormal neuroanatomy | embryonic stage 16 phenotype of Abl4
sli[+]/sli1 is an enhancer of abnormal neuroanatomy | embryonic stage 16 | dominant phenotype of robo11
robo15, sli[+]/sli1 has abnormal neuroanatomy | dominant | embryonic stage 16 phenotype
robo[+]/robo15, sli1 has abnormal neuroanatomy phenotype
robo15, sli[+]/sli1 has abnormal neuroanatomy phenotype
robo15, sli1 has abnormal neuroanatomy phenotype
robo15, sli1 has abnormal neuroanatomy | dominant phenotype
robo[+]/robo15, sli1 has abnormal neuroanatomy | dominant phenotype
robo15, sli[+]/sli1 has abnormal neuroanatomy | dominant phenotype
robo15, sli[+]/sli1 has larval longitudinal connective | embryonic stage 16 phenotype, enhanceable by kuzH143
robo15, sli[+]/sli1 has commissure | embryonic stage 16 phenotype, enhanceable by kuzH143
robo15, sli[+]/sli1 has larval longitudinal connective | embryonic stage 16 phenotype, enhanceable by kuz112
robo15, sli[+]/sli1 has commissure | embryonic stage 16 phenotype, enhanceable by kuz112
robo15, sli[+]/sli1 has larval longitudinal connective | embryonic stage 16 phenotype, enhanceable by kuze29-4
robo15, sli[+]/sli1 has commissure | embryonic stage 16 phenotype, enhanceable by kuze29-4
robo15, sli1 has medial longitudinal fascicle phenotype, enhanceable by RhoGAP93BRNAi.UAS.cBa/Scer\GAL4elav.PLu
robo15, sli1 has larval MP1 neuron phenotype, enhanceable by dock04723
robo15, sli1 has larval longitudinal connective phenotype, enhanceable by dock04723
robo15, sli1 has pCC neuron phenotype, enhanceable by dock04723
robo15, sli1 has larval longitudinal connective phenotype, enhanceable by dock3
robo15, sli1 has larval longitudinal connective phenotype, enhanceable by PakUAS.Tag:MYC/Scer\GAL4elav.PLu
robo15, sli1 has larval longitudinal connective phenotype, enhanceable by Scer\GAL4elav.PLu/PakUAS.Tag:Myr(Src64B)
robo11, sli[+]/sli1 has larval longitudinal connective | embryonic stage 16 phenotype, enhanceable by Abl4/Abl[+]
sli1 has larval longitudinal connective | embryonic stage 16 phenotype, enhanceable by Abl4/Abl[+]
sli1 has larval longitudinal connective | embryonic stage 16 phenotype, enhanceable by AblUAS.cHa/Scer\GAL4elav.PLu
sli1 has larval longitudinal connective | embryonic stage 16 phenotype, enhanceable by Scer\GAL4elav.PLu/Abl::Hsap\ABL1::Hsap\BCRP210.UAS
sli1 has larval longitudinal connective | embryonic stage 16 phenotype, enhanceable by Abl::Hsap\ABL1::Hsap\BCRKR.UAS/Scer\GAL4elav.PLu
robo15, sli[+]/sli1 has larval anterior commissure phenotype, enhanceable by Scer\GAL4elav-C155/Nedd4UAS.Tag:MYC
robo15, sli[+]/sli1 has larval posterior commissure phenotype, enhanceable by Scer\GAL4elav-C155/Nedd4UAS.Tag:MYC
robo15, sli[+]/sli1 has larval ventral nerve cord phenotype, enhanceable by Scer\GAL4elav-C155/Nedd4UAS.Tag:MYC
robo15, sli[+]/sli1 has larval longitudinal connective phenotype, enhanceable by AblEP3101/Scer\GAL4elav.PLu
robo15, sli[+]/sli1 has larval longitudinal connective phenotype, enhanceable by ena[+]/enaGC1
robo15, sli[+]/sli1 has larval longitudinal connective phenotype, enhanceable by ena[+]/enaGC5
robo15, sli[+]/sli1 has larval longitudinal connective phenotype, enhanceable by ena[+]/enaGC8
sli1 has larval longitudinal connective phenotype, enhanceable by AblEP3101/robo15/Scer\GAL4elav.PLu
sli1 has larval longitudinal connective phenotype, enhanceable by robo[+]/robo15
sli1 has larval longitudinal connective phenotype, enhanceable by robo[+]/ena[+]/enaGC1/robo15
sli1 has larval longitudinal connective phenotype, enhanceable by robo[+]/ena[+]/enaGC5/robo15
sli1 has larval longitudinal connective phenotype, enhanceable by robo[+]/ena[+]/enaGC8/robo15
robo[+]/robo15, sli1 has commissure phenotype, non-enhanceable by tutl[+]/tutlex383
robo15, sli[+]/sli1 has commissure phenotype, non-enhanceable by tutl[+]/tutlex383
robo15, sli1 has medial longitudinal fascicle phenotype, non-enhanceable by RacGAP84CUAS.cRa/Scer\GAL4elav.PLu
robo15, sli1 has medial longitudinal fascicle phenotype, non-enhanceable by RhoGAP100FRNAi.UAS.cBa
robo15, sli1 has medial longitudinal fascicle phenotype, non-enhanceable by CdGAPrRNAi.UAS
robo15, sli1 has medial longitudinal fascicle phenotype, non-enhanceable by RhoGAP19DRNAi.UAS.cBa
robo15, sli1 has medial longitudinal fascicle phenotype, non-enhanceable by tumRNAi.UAS.cBa
robo15, sli[+]/sli1 has larval longitudinal connective phenotype, suppressible by Abl1/Abl[+]
robo15, sli[+]/sli1 has larval longitudinal connective phenotype, suppressible by Abl4/Abl[+]
sli1 has larval longitudinal connective phenotype, suppressible by robo[+]/Abl1/robo15/Abl[+]
sli1 has larval longitudinal connective phenotype, suppressible by robo[+]/Abl4/robo15/Abl[+]
robo[+], sli[+], robo15, sli1 is an enhancer of larval longitudinal connective | embryonic stage 16 phenotype of kuze29-4
robo[+], sli[+], robo15, sli1 is an enhancer of commissure | embryonic stage 16 phenotype of kuze29-4
robo[+], sli[+], robo15, sli1 is an enhancer of larval longitudinal connective | embryonic stage 16 phenotype of kuzH143
robo[+], sli[+], robo15, sli1 is an enhancer of commissure | embryonic stage 16 phenotype of kuzH143
sli[+]/sli1 is an enhancer of larval longitudinal connective | embryonic stage 16 phenotype of Abl4
sli[+]/sli1 is an enhancer of larval longitudinal connective | embryonic stage 16 phenotype of robo11
sli[+]/sli1 is an enhancer of presumptive embryonic/larval central nervous system phenotype of sim2
sli[+]/sli1 is an enhancer of larval longitudinal connective phenotype of sim2
sli[+]/sli1 is an enhancer of presumptive embryonic/larval central nervous system phenotype of jing01094
robo15, sli[+]/sli1 has commissure | embryonic stage 16 phenotype
robo15, sli[+]/sli1 has larval longitudinal connective | embryonic stage 16 phenotype
robo15, sli[+]/sli1 has commissure phenotype
robo[+]/robo15, sli1 has commissure phenotype
robo15, sli1 has medial longitudinal fascicle phenotype
robo15, sli1 has larval longitudinal connective phenotype
robo15, sli1 has pCC neuron phenotype
robo15, sli1 has larval MP1 neuron phenotype
robo15, sli1 has larval ventral nerve cord phenotype
robo15, sli1 has larval anterior commissure phenotype
robo15, sli1 has larval posterior commissure phenotype
robo[+]/robo15, sli1 has larval ventral nerve cord phenotype
robo[+]/robo15, sli1 has larval anterior commissure phenotype
robo[+]/robo15, sli1 has larval posterior commissure phenotype
robo15, sli[+]/sli1 has larval anterior commissure phenotype
robo15, sli[+]/sli1 has larval posterior commissure phenotype
jing01094, sli1 has presumptive embryonic/larval central nervous system phenotype
jing01094, sli1 has ventral midline of embryo phenotype
jing01094, sli[+]/sli1 has ventral midline of embryo phenotype
sim2, sli1 has ventral midline of embryo phenotype
sim2, sli[+]/sli1 has ventral midline of embryo phenotype
sim2/sim[+], sli1 has presumptive embryonic/larval central nervous system phenotype
sim2/sim[+], sli1 has ventral midline of embryo phenotype
jing[+]/jing01094, sli1 has presumptive embryonic/larval central nervous system phenotype
jing[+]/jing01094, sli1 has ventral midline of embryo phenotype
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.
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.
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.
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.
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.