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General Information
Symbol
Dmel\sli2
Species
D. melanogaster
Name
FlyBase ID
FBal0015700
Feature type
allele
Associated gene
Associated Insertion(s)
Carried in Construct
Also Known As
slit2, sliIG107, slitIG107
Nature of the Allele
Mutations Mapped to the Genome
 
Type
Location
Additional Notes
References
point mutation
Nucleotide change:

A15875495T

Reported nucleotide change:

A3150T

Amino acid change:

K1024term | sli-PA; K1024term | sli-PB; K1048term | sli-PC; K1024term | sli-PD; K1048term | sli-PE; K1048term | sli-PF

Reported amino acid change:

K?term

Associated Sequence Data
DNA sequence
Protein sequence
 
 
Progenitor genotype
Cytology
Nature of the lesion
Statement
Reference

Nucleotide substitution: A3150T.

Amino acid replacement: K?term.

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

axon & pCC neuron

chordotonal organ & axon | lateral

chordotonal organ & embryo & nerve terminal

eye photoreceptor cell & axon (with slik04807b)

mesothoracic dorsal triscolopidial chordotonal organ dch3 & scolopidial dendrite

metathoracic dorsal triscolopidial chordotonal organ dch3 & scolopidial dendrite

Detailed Description
Statement
Reference

sli2 homozygous embryos exhibit severe axon guidance defects in the longitudinal connective as early as 9h post-fertilization - e.g. growth cones of posterior corner cell neurons tangentially projected towards the midline -, as compared to controls.

The adult brain of sli2/slik04807b transheterozygotes exhibits major defects in neuropil organization in several central brain areas including the central complex, mushroom body lobes, antennal lobes and Robo2/Robo3-expressing axons, as compared to either heterozygous controls; their adult sLNv neurons exhibit significantly longer axon projections compared to controls.

The adult sLNv neurons of sli2 heterozygotes that also express sliJF01229 under the control of Scer\GAL4ey-OK107 (in combination with Dicer-2, for efficient RNAi) exhibit significantly longer axon projections compared to controls.

sli2 homozygous embryonic heart cardioblasts show a rounded morphology, show significant decreases in migration velocity, as well as in filopodial and lamellopodial extensions and activities, as compared to controls; these are associated with gaps in the leading edge (and lost adhesions with ipsilateral partners), cell clumping, improper linear alignment of the cardioblasts, and embryonic heart lumen formation defects, as compared to controls. sli2 heterozygous cardioblasts also show a significant decrease in filopodial activity, but not in lamellopodial activity or migration velocity, as compared to controls.

In sli2/+ embryos, the normally ipsilateral-projecting ap-positive neurons display occasional defects.

Tracheal dorsal branch fusion occurs normally in the tracheal system of sli2/+ third instar larvae

sli2/Df(2R)Jp5 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.

Mild ectopic ap neuron crossing defects are seen in heterozygous sli2 stage 16 embryos.

In sli2 mutant embryos the ventral longitudinal muscles cross dorsally over the CNS, meeting those from the other side to form ectopic muscle attachments along the ventral midline.

In sli2 mutant embryos, the entire axon scaffold collapses at the midline. The Scer\GAL4ap-md544-expressing axons project directly to the midline and do not leave.

Many of the dorsal abdominal clusters in sli2 mutant animals have branches that exceed the normal level of extension at approximately 21 and 22 hours after egg laying. The maximal dendrite length with respect to the most dorsally positioned neuronal cell body is significantly altered in mutants.

Class IV sli2 mutant neurons display dendrite over-elongation and reduced branching. Class IV neurons show less high order branches and form longer dendrite process compared to control embryos. The number of branches of class IV neurons is significantly decreased in robo1 mutants at 22 hours after egg laying. The dorsal elongation and the average branch length are significantly increased.

sli2/+ embryos show a mild axon guidance defect of the Apterous neurons; less than one thick bundle of Ap neurons cross the midline on average per sli2/+ embryo, while these neurons never cross in wild-type embryos.

In robo2 embryos, the pCC axons aberrantly cross the midline.

sli2 mutant embryos present a very severe fused commissure phenotype.

sli2 embryos show defective heart development. These embryos have breaks in the continuity of the adherent cardial cells during migration, which can lead to lesions in the final heart vessel. Sometimes, a few cardial cells are not incorporated into the heart, nuclei sometimes cross the midline and irregular bulges in cardial alignment are produced. The hearts of sli2 embryos have either no lumen, or a very small one, and an expanded basolateral zone. Dorsal closure is not affected in these mutants.

sli2/+ mutants have a normal heart.

Although the appropriate number of cardioblasts are specified in sli2 embryos, cell adhesion between cardioblasts is lost. Thus, in 97% of sli2 embryos, the cardioblasts fail to form two continuous rows of cells, showing frequent gaps and inappropriate cell clustering and intermingling with the flanking pericardial cells: approximately 104 Mef2-positive cardioblast nuclei form two rows at the dorsal midline in wild type embryos, whereas there are only approximately 87.9 Mef2-positive cells at this position in sli2 mutant embryos. The rows of pericardial cells that flank the rows of cardioblasts are also misaligned in sli2 embryos, and often show gaps that frequently correspond with the gaps in the rows of cardioblasts.

The shape of cardioblasts in sli2 embryos is abnormal.

90% of sli2 embryos have salivary glands that curve medially towards the CNS midline, instead of lying parallel to the midline in the wild-type position.

When the bilateral rows of myocardial progenitors have reached the dorsal midline, they fail to align properly in sli2 mutants compared to wild-type. There are two types of myocardial cell misalignments: type I consist of irregularities in the myocardial cell rows and type II, in addition, has gaps and triple lines of myocardial cells. The apical-lateral polarity of the heart tube is disrupted in sli2 mutants.

Normal separation of primordial germ cells into lateral clusters on each side of the embryo is observed in homozygous and heterozygous sli2.

33% of thoracic segments show transformation of the dch3 chordotonal organs to a morphology resembling that of abdominal lch5 chordotonal organs in mutant embryos; the transformed "dch3" organs are positioned laterally and have dendrites pointing dorsally.

The vp1-4a external sensory organs in the abdomen are correctly specified and positioned in stage 16 mutant embryos. However, the ventral multidendritic (vmd) neuron cluster contains a variable number of md neurons, ranging from 4 (one md neuron missing in 29% of hemisegments) to 6 (one extra md neuron in 24% of hemisegments). The variation in number of neurons in the vmd cluster is due to variation in the number of vmd1a neurons in the cluster (the wild-type vmd cluster contains 1 vmd1a neuron). By comparing the vmd cluster on each side of the midline in a segment, it is seen that whenever two vmd1a neurons are seen in one hemisegment, no vmd1a neuron is seen in the contralateral hemisegment, strongly suggesting that the vmd1a neuron can cross the midline in these embryos. In 3 segments, the loss of the vmd1a neuron did not correlate with its duplication in the contralateral hemisegment. In these cases, the missing vmd1a neuron has probably remained at the midline. Analysis of the position of the vmd1a neuron and its precursor cells in sli2 mutant embryos at different stages indicates directly that the vmd1a neuron can cross the midline in these embryos.

Most of ventral muscles cross the midline in homozygous embryos. The Fas2-positive fascicles are collapsed into the ventral midline at stages 16 and 17. 0.6% of inner Fas2-positive fascicles cross the ventral midline in heterozygous embryos.

slik04807b/sli2 third instar larvae show defects in photoreceptor axon targeting, with gaps in the lamina and increased numbers of axons entering the medulla. slik04807b/sli2 animals show disruption of the lamina glia layer; clumps of glia and gaps in the glial layers are seen. The regions of photoreceptor axon mistargeting correlate with areas of lamin glial disruption. Many distal cell neurons enter the base of the lamina in slik04807b/sli2 third instar larvae and some distal cell neurons invade the lamina neuropil, disrupting photoreceptor innervation.

Heterozygous mutants do not exhibit significant longitudinal axon ectopic midline crossing defects.

lch5 axons stall before turning point TP1 in 10% of hemisegments or misproject to the v'ch1 pathway in 12% of hemisegments of mutant embryos. Dorsal cluster axons stall in the lateral region of the embryo in 10% of hemisegments or project in abnormal directions (usually after reaching the lateral region) in 8% of hemisegments. Mutant embryos have defects in the tracheal system, including the spiracular branch and transverse connective. Motor axon projections are often disrupted in mutant embryos. In mutant hemisegments which have a normal location of the spiracular branch, normal position and orientation of the dorsal and lateral sensory neuron cell bodies and normal motor axon trajectories, 14% of the hemisegments have lch5 axons projecting to the v' pathway and 28% of hemisegments have lesA/ldaA axons projecting to the v' pathway, while the dorsal cluster axons follow a normal trajectory to the lateral region in all the hemisegments.

Homozygous embryos show three Fas2 fascicles collapsed on the midline. The ch neurons project across the midline and either stall or reach as far as the outer far edge of the CNS. Either way they fail to branch.

Heterozygous embryos only extremely rarely show Fas2-expressing axons crossing the midline.

One or two Fas2-positive axon bundles cross the midline in about 36% of heterozygous embryos.

sli2 heterozygotes exhibit 3.4% midline errors (as assayed with Fas2).

Heterozygotes show 4% ectopic crossing of the midline by axons in the embryonic central nervous system.

1.0% of expected mutant embryos hatch as first instar larvae. The latest observed stage of mutants is L1. Nerve cord length is 88% of embryo length. Midline guidance failure of repellence phenotype, evidenced by midline crossing, is severe. Mutant embryos show complete fusion of the longitudinal and commissural nerve trunks - few intersegmental connections are maintained. 6.8 ventral oblique muscles per segment remain on the dorsal surface of the ventral nerve cord, instead of having migrated to the edges and inserted into the ectoderm.

All CNS axons converge on the midline which is displaced ventrally.

sli2 embryos in which the midline has been rescued by expressing sliScer\UAS.cKa under the control of Scer\GAL4sim.P3.7 often show misinsertion of dorsal muscles 1,2, 9 and 10. However, the overall position of these muscles is not dramatically affected in these embryos. Muscles 21 to 23 are largely unaffected although occasionally an extra muscle is seen. 1% of segments show crossing of the midline by muscles 6/7, 54% show abnormal insertion of muscle 5 and 36% show abnormal insertion of muscles 6/7 (either failing to reach their specific muscle insertion sites in the epidermis - 12%, or reaching the epidermis but making abnormal connections - 24%). In sli2 embryos expressing sliScer\UAS.cKa under the control of Scer\GAL4en-e16E, 49% of segments show muscle cells aligned with sites of ectopic sli expression. In sli2 embryos expressing sliScer\UAS.cKa under the control of Scer\GAL4ptc-559.1, 20% of segments show muscle cells aligned with sites of ectopic sli expression. Ventral longitudinal muscles 6 and 7 cross the midline in 90% of segments in mutant embryos. Muscle 13 also occasionally crosses the midline. Muscle 5 is present, although it is frequently attached to the wrong site in the epidermis.

The ventral muscles fail to migrate away from the midline in mutant embryos, resulting in muscles that extend over the dorsal surface of the CNS. The initial migration defect seen in the ventral muscle precursors of sli2 embryos is rescued by expression of sliScer\UAS.cKa under the control of Scer\GAL4sim.P3.7. However, striking defects are seen during the second phase, as muscles extend towards their (muscle attachment sites) MASs. Many muscles that normally attach at sli-positive MASs are instead attached to the wrong places in the epidermis. Muscles 6 and 7 either do not reach their MASs or make abnormal connections with the epidermis. Muscle 5 is often missing or is not properly attached at one or both ends. Muscle 4 is also often not properly attached.

The GMC-1 in mutants frequently (about 10%) divide symmetrically to generate two RP2s instead of an RP2 and a sib.

Approximately 24% of heterozygous embryos show periodic crossovers of Fas2-positive axons across the midline.

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

All axons in the longitudinal connectives are collapsed towards a single midline tract. MP pioneers are medially displaced in stage 12/0 mutant embryos. Contralaterally projecting axons persist in sli mutants despite fusion of longitudinal tracts. Midline glia are displaced to the ventral limit of the neuropil, and maintain contact with commissural axons. Anterior and posterior to the commissural axons the neuropil of sli mutant nerve cords contains many more growth cone filopodia, and fewer axons than wild type. The longitudinal connectives appear to recross the midline as they project anteriorly or posteriorly, similarly to robo mutants. Most mesectodermal cells line the ventral midline. The ventral oblique muscles do not insert below the cord, but cross the dorsal surface of the cord and insert contralaterally with the ventral longitudinal muscles. When the mutant phenotype is partially rescued by the sliScer\UAS.cBa, Scer\GAL4sim.P3.7 combination, midline structures are partially restored, but errant axons continue to cross the midline. This phenoytpe is comparable to that of sli532 or a robo hypomorph. Mesectodermal cytoarchitecture is not restored. Embryos heterozygous for either robo1 or sli2 show deviation of longitudinal fascicles towards the midline in less than 5% of segments.

Axons enter the midline, but fail to leave it and instead run along it in one longitudinal tract in the central nervous system (CNS) of sli2 embryos. The pCC axon aberrantly enters the midline in homozygous embryos, where it fasciculates with its contralateral homologue. The pCC homologues then extend anteriorly along the midline. In some segments the aCC axon crosses the midline and fasciculates with the axon of its contralateral homologue (in contrast to wild-type where it normally extends ipsilaterally away from the midline). Commissural axons such as SP1 do not leave the midline. The ventral muscles extend over the dorsal surface of the CNS.

In stage 13 embryos the dorsal median cells are mislocalised to lateral positions away from the midline. By stage 16 the cells are absent from most segments.

Mutant phenotype as assayed by Ecol\lacZrp staining: midline missing. Mutant phenotype of lateral chordotonal axons includes: shorter axons, defasciculated axons or dorsally routed axons.

In stage 12/3 homozygous embryos the commissures are pioneered but are closer together than wild type. By stage 14 the longitudinal tracts have collapsed at the midline. Midline glia reach the dorsal midline by stage 12/5, become ventrally displaced during stage 13 and by stage 14 are spread from the dorsal to ventral surface. VUM neurons are present at the proper position during stage 11 by are misplaced ventrally by stage 13. These neurons are still present at the ventral midline at stage 14. In stage 13 embryos the wild-type number of MP1 neurons are present but displaced ventrally, by stage 14 they are fused at the midline. en+ neurons are present at stage 14 but are displaced.

Longitudinal tracts fuse at the ventral midline, though the glial scaffold is normal.

Absence of commissures and the collapse of the longitudinal tracts into a single fused tract at the midline. The midline precursor cells are displaced ventrally and do not differentiate properly. The posterior commissure sometimes forms and the anterior commissure is always initially formed, but the commissures are narrower and are not as straight or regular in shape. The commissures disappear as the midline precursors displace.

The presence of Ecol\lacZsim.7.8 construct shows that the midline cells are disorganised compared to wild type at stage 11 and at stage 13 are clustered near the ventral surface of the embryo leading to the collapse of the two lateral CNS hemiganglia and fusion of the longitudinal connectives.

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

robo[+]/robo11, sli2 has neuroanatomy defective phenotype, enhanceable by β-Specem6

robo[+]/robo11, sli2 has neuroanatomy defective phenotype, enhanceable by β-SpecG0074

robo[+]/robo11, sli2 has neuroanatomy defective phenotype, enhanceable by β-SpecG0198

sli2 has neuroanatomy defective | embryonic stage phenotype, enhanceable by exba[+]/kra2

sli2 has neuroanatomy defective | embryonic stage phenotype, enhanceable by shot3/shot[+]

shot3/shot[+], sli2 has neuroanatomy defective | embryonic stage phenotype, enhanceable by exba[+]/kra2

sli2 has neuroanatomy defective phenotype, enhanceable by capt10/capt[+]

sli2 has neuroanatomy defective phenotype, enhanceable by Abl2/Abl[+]

sli2 has neuroanatomy defective phenotype, enhanceable by capt[+]/captB99

sli2 has neuroanatomy defective phenotype, enhanceable by captk01217/capt[+]

NOT Enhanced by
Suppressed by
NOT suppressed by
Statement
Reference
Enhancer of
Statement
Reference

sli2/sli[+] is an enhancer of neuroanatomy defective phenotype of communspecified

sli2, robo[+], robo11 is an enhancer of neuroanatomy defective phenotype of β-Specem6

sli2, robo[+], robo11 is an enhancer of neuroanatomy defective phenotype of β-SpecG0074

sli2, robo[+], robo11 is an enhancer of neuroanatomy defective phenotype of β-SpecG0198

sli2/sli[+] is an enhancer of neuroanatomy defective phenotype of elav5

sli2/sli[+] is an enhancer of neuroanatomy defective phenotype of Sdcunspecified

sli2/sli[+] is an enhancer of neuroanatomy defective phenotype of lolaORE120

NOT Enhancer of
Statement
Reference

sli2/sli[+] is a non-enhancer of neuroanatomy defective | dominant | adult stage phenotype of tapGal4

sli2/sli[+] is a non-enhancer of neuroanatomy defective phenotype of egh7

Suppressor of
NOT Suppressor of
Statement
Reference
Other
Statement
Reference
Phenotype Manifest In
Enhanced by
Statement
Reference

sli2 has embryonic heart cardioblast phenotype, enhanceable by robo11/robo1[+]

sli2 has filopodium | embryonic stage phenotype, enhanceable by robo11/robo1[+]

sli2 has axon & pCC neuron phenotype, enhanceable by exba[+]/kra2

sli2 has axon & pCC neuron phenotype, enhanceable by shot3/shot[+]

shot3/shot[+], sli2 has axon & pCC neuron phenotype, enhanceable by exba[+]/kra2

sli2 has heart primordium phenotype, enhanceable by mys1/mys[+]

sli2 has heart primordium phenotype, enhanceable by scb[+]/scb01288

sli2 has heart primordium phenotype, enhanceable by LanA9-32/LanA[+]

sli2 has heart primordium phenotype, enhanceable by wb[+]/wbSF11

sli2 has heart primordium phenotype, enhanceable by vkg177/vkg[+]

sli2 has heart primordium phenotype, enhanceable by vkg[+]/vkgP10038

sli2 has heart primordium phenotype, enhanceable by rhea[+]/rhea1

sli2 has heart primordium phenotype, enhanceable by lea[+]/robo2lea-2

sli2 has heart primordium phenotype, enhanceable by lea[+]/robo2S4-18

sli2 has heart primordium phenotype, enhanceable by Nrt[+]/NrtM54

sli2 has heart primordium phenotype, enhanceable by Ras85D05703/Ras85D[+]

sli2 has heart primordium phenotype, enhanceable by Ilk[+]/IlkZCL3111

sli2 has fascicle phenotype, enhanceable by dock04723

sli2 has ventral nerve cord phenotype, enhanceable by robo[+]/robo11

sli2 has longitudinal connective phenotype, enhanceable by robo[+]/robo11

NOT Enhanced by
Statement
Reference

sli2 has lamellipodium | embryonic stage phenotype, non-enhanceable by robo11/robo1[+]

sli2 has heart primordium phenotype, non-enhanceable by mew[+]/mewM6

sli2 has heart primordium phenotype, non-enhanceable by Tigx/Tig[+]

sli2 has heart primordium phenotype, non-enhanceable by dock[+]/dock04723

Suppressed by
NOT suppressed by
Enhancer of
Statement
Reference

sli2/sli[+] is an enhancer of filopodium | embryonic stage phenotype of robo11

sli2/sli[+] is an enhancer of lamellipodium | embryonic stage phenotype of robo11

sli2/sli[+] is an enhancer of longitudinal connective phenotype of communspecified

sli2, robo[+], robo11 is an enhancer of medial longitudinal fascicle | ectopic phenotype of β-Specem6

sli2/sli[+] is an enhancer of commissure phenotype of elav5

sli2/sli[+] is an enhancer of embryo | dorsal closure stage phenotype of scb01288

sli2/sli[+] is an enhancer of chordotonal organ & embryo & nerve terminal phenotype of robo31

sli2/sli[+] is an enhancer of longitudinal connective phenotype of lolaORE120

sli2 is an enhancer of fascicle phenotype of mys1

sli2 is an enhancer of fascicle phenotype of robo1unspecified

sli2 is an enhancer of fascicle phenotype of mewM6

sli2 is an enhancer of fascicle phenotype of scbunspecified

sli2 is an enhancer of fascicle phenotype of dock04723

sli2/sli[+] is an enhancer of longitudinal connective phenotype of robo11

NOT Enhancer of
Statement
Reference

sli2/sli[+] is a non-enhancer of adult mushroom body beta-lobe | adult stage phenotype of tapGal4

sli2/sli[+] is a non-enhancer of photoreceptor cell R1 & axon phenotype of egh7

sli2/sli[+] is a non-enhancer of photoreceptor cell R2 & axon phenotype of egh7

sli2/sli[+] is a non-enhancer of photoreceptor cell R3 & axon phenotype of egh7

sli2/sli[+] is a non-enhancer of photoreceptor cell R4 & axon phenotype of egh7

sli2/sli[+] is a non-enhancer of photoreceptor cell R5 & axon phenotype of egh7

sli2/sli[+] is a non-enhancer of photoreceptor cell R6 & axon phenotype of egh7

Suppressor of
Statement
Reference

sli2/sli[+] is a suppressor of wing phenotype of if3

NOT Suppressor of
Statement
Reference

sli2/sli[+] is a non-suppressor of photoreceptor cell R6 & axon phenotype of egh7

sli2/sli[+] is a non-suppressor of photoreceptor cell R1 & axon phenotype of egh7

sli2/sli[+] is a non-suppressor of photoreceptor cell R2 & axon phenotype of egh7

sli2/sli[+] is a non-suppressor of photoreceptor cell R3 & axon phenotype of egh7

sli2/sli[+] is a non-suppressor of photoreceptor cell R4 & axon phenotype of egh7

sli2/sli[+] is a non-suppressor of photoreceptor cell R5 & axon phenotype of egh7

Other
Statement
Reference

Ptp69D1/Ptp69D[+], sli2 has axon | adult stage phenotype

dlg1[+]/dlg11, sli2 has cardioblast phenotype

shg[+]/shg2, sli2 has cardioblast phenotype

Dg248/Dg[+], sli2 has cardioblast phenotype

Additional Comments
Genetic Interactions
Statement
Reference

The expression of robo2UAS.EGFP leads to shorter sLNv neuron projections (Scer\GAL4Pdf.PU-driven expression) and to the absence of the normal DCN neuron commissure (Scer\GAL4ato.PU-driven expression), both of which are suppressed by sli2/slik04807b transheterozygosity.

The adult sLNv neurons of sli2, Ptp69D1 double heterozygotes exhibit significantly longer axon projections compared to controls.

sli2, robo11 double heterozygotes show a more severe decrease in filopodial activity compared to either single heterozygote conditions and a more severe decrease in lamellopodial activity compared to robo11 heterozygotes, but do not show significant changes in migration velocity compared to controls.

sli2/+ does not significantly enhance frequency of mushroom body beta lobe axon overgrowth defects in tapGal4/+ brains.

Expression of AblScer\UAS.T:Avic\GFP in ap neurons, under the control of Scer\GAL4ap-md544 enhances the axon crossing defects found in sli2/+ mutant embryos.

Expression of AblN.Scer\UAS.T:Avic\GFP in ap neurons, under the control of Scer\GAL4ap-md544 enhances the axon crossing defects found in sli2/+ mutant embryos, indicating the C-terminal portion of Abl is not involved in this interaction.

Expression of AblΔFABD.Scer\UAS.T:Avic\GFP in ap neurons, under the control of Scer\GAL4ap-md544 does not enhance the axon crossing defects found in sli2/+ mutant embryos.

Expression of AblR297K.Scer\UAS.T:Avic\GFP in ap neurons, under the control of Scer\GAL4ap-md544 does not enhance the axon crossing defects found in sli2/+ mutant embryos.

sli2/+ Sac11/+ double heterozygotes show a high frequency of ectopic midline crossings in the central nervous system.

sli2/+ suppresses the dorsal branch fusion phenotype seen when SdcdsRNA.Scer\UAS.cSa is expressed under the control of Scer\GAL4btl.PS.

One copy of sli2 partially suppresses the dorsal branch fusion phenotype seen in the tracheal system of Sdc2639 homozygous third instar larvae. One copy each of sli2 and Sdc2639 does not produce any dorsal branch fusion defects.

kuzH143, sli2 transheterozygous stage 16 embryos display a stronger ectopic ap neuron crossing phenotype than either mutant alone.

kuz2583/+ enhances the ectopic ap neuron crossing phenotype seen in sli2 heterozygous stage 16 embryos.

kuz112/+ enhances the ectopic ap neuron crossing phenotype seen in sli2 heterozygous stage 16 embryos.

Expression of kuzDN.Scer\UAS in ipsilateral ap neurons under the control of Scer\GAL4ap-md544 in a sli2/+ mutant background produces more severe ap axon midline crossing defects in stage 16 embryos than in either mutant alone.

Blocking vg function through expression of sdΔ88-159.Scer\UAS in ventral longitudinal muscle cells (under the control of Scer\GAL4Mef2.PR) that abnormally migrate along the midline owing to a sli2 mutant background, leads to fewer and smaller muscle-muscle adhesions.

Increasing vg function through expression of vg2.Scer\UAS in ventral longitudinal muscle cells (under the control of Scer\GAL4Mef2.PR) that abnormally migrate along the midline owing to a sli2 mutant background, leads to more and larger muscle-muscle adhesion sites.

Increasing vg function through expression of vg2.Scer\UAS in somatic muscle cells (under the control of Scer\GAL4Mef2.PR) of sli2 mutants greatly enhances the adhesion level between the midline-crossing ventral longitudinal muscles.

Expression of EgfrDN.Scer\UAS in somatic muscle cells (under the control of Scer\GAL4Mef2.PR) of sli2 mutants decreases the size and/or number of adhesion sites along the midline.

High levels of Scer\GAL4ap-md544>leaEP expression are insufficient to direct Scer\GAL4ap-md544-expressing axons away from the midline in a sli2 mutant genetic background.

One copy of sli2 weakly suppresses the detached posterior crossvein phenotype seen when DysdsRNA.NH2.Scer\UAS is expressed under the control of Scer\GAL4Act.PU.

One copy of sli2 weakly suppresses the detached posterior crossvein phenotype seen when DysdsRNA.C.Scer\UAS is expressed under the control of Scer\GAL4tub.PU but produces extra wing vein material.

The longitudinal tract midline crossing phenotype seen in communspecified mutants is significantly enhanced by sli2/+, both in terms of the numbers of segments and the number of embryos affected.

sli2, robo1/+ embryos show midline axon guidance defects, with on average two to three medial longitudinal fascicle ectopically crossing the midline per embryo.

β-Specem6/Y; sli2, robo1/+ show an enhancement of the midline axon guidance defects seen in β-Specem6/Y and sli2, robo1/+ embryos as more medial longitudinal fascicles ectopically cross the midline in the triple mutant. An enhancement is also seen in β-SpecG0074/Y; sli2, robo1/+ and β-SpecG0198/Y; sli2, robo1/+ triple mutant embryos. Expression of β-SpecScer\UAS.T:Hsap\MYC, under the control of Scer\GAL4elav.PLu, rescues the phenotype of the triple mutants back to the milder phenotype seen in sli2, robo1/+ embryos.

The Apterous neuron axon guidance phenotype of sli2/+ embryos is enhanced in β-Specem6/Y; sli2/+ and β-SpecG0198/Y; sli2/+ embryos, although the timing at which the defects appear is not altered. Expression of β-SpecScer\UAS.T:Hsap\MYC under the control of Scer\GAL4ap-md544 is unable to rescue the β-Specem6/Y; sli2/+ phenotype back to the sli2/+ severity.

Expression of fraΔC.Scer\UAS.T:Ivir\HA driven by Scer\GAL4elav.PLu in a fraunspecified sli2 double mutant background results in a phenotype similar to the phenotype observed for overexpression of fraΔC.Scer\UAS.T:Ivir\HA in a fraunspecified single mutant background, where many axons fail to cross the midline.

The axon midline phenotype of sli2/+ embryos is enhanced in sli2/+; exba2/+ and shot3/+, sli2/+ double mutants. The phenotype is further enhanced in shot3/+, sli2/+; exba2/+ triple mutants.

Reduction of sli in a sli2 heterozygous background leads to a fused commissures phenotype in elav5 mutant embryos.

The sli2 heart development phenotype is enhanced by the following alleles, as judged by the appearance of defective heart formation in doubly heterozygous embryos: mys1, scb01288, LanA9-32, wbSF11, vkg177, vkgP10038 and rhea1. The following alleles produce a mild heart phenotype when doubly heterozygous with lea2, leaS4-18, NrtM54 and Ras85D05703.

IlkZCL3111/+; sli2/+ embryos show defects in heart formation including delays in midline fusion of cardial cells, which suggests a delay in dorsal closure.

The following doubly heterozygous embryos show no defects in heart formation: mewM6/+; sli2/+ embryos, Tigx/+, sli2/+ embryos and dock04723/+, sli2/+ embryos.

Dorsal closure is delayed in sli2/+, scb01288/+ embryos but is complete at hatching.

In egh7/Y; sli2/+ mutants, the R-cell axonal projection pattern is defective like in egh7 single mutants. egh7/+; sli2/+ mutants appear wild type.

In robo1,sli2 /+,+ stage 16 embryos, FasII axons cross the midline in three to five segments per embryo.

Expression of Nedd4Scer\UAS.T:Hsap\MYC under the control of either Scer\GAL4elav.PLu or Scer\GAL41407 does not enhance the midline crossing phenotype seen in transheterozygous sli2 robo1 stage 16 embryos.

Expression of Nedd4EY00500 under the control of either Scer\GAL4elav.PLu or Scer\GAL41407 does not enhance the midline crossing phenotype seen in transheterozygous sli2 robo1 stage 16 embryos.

Df(3R)ED4688 does not enhance the midline crossing phenotype seen in transheterozygous sli2 robo1 stage 16 embryos.

Expression of enaScer\UAS.cCa under the control of Scer\GAL4elav.PLu suppresses the midline crossing phenotype seen in transheterozygous sli2 robo1 stage 16 embryos.

In sli2; fra3/fra4 double mutants, the penetrance of the salivary gland guidance defects is reduced by 40% compared to sli2 single mutants.

The following mutations cause defective cardiac cell alignment when heterozygous in combination with sli2/+: Dg248, dlg11, shg2 and Df(2R)Jp6. In contrast, 96% of sli2/+, crb2/+ embryos show normal cardiac cell alignment.

The transformation of abdominal lch5 chordotonal organs to a morphology resembling thoracic dch3 chordotonal organs that is seen in larvae expressing leaEP2582 under the control of Scer\GAL4elav-C155 is attenuated if the larvae also carry one copy of sli2; only 17.2% of abdominal segments have partial or complete transformation of the lch5 organs in the double mutant larvae at 25oC.

sli2 chb4 double heterozygous embryos have axons ectopically crossing the midline. sli2 chbP4 double heterozygous embryos have axons ectopically crossing the midline.

The abnormal crossing of the midline by the vmd1a neuron of the ventral multidendritic neuron cluster that is seen in sli2 embryos still occurs if the embryos are also homozygous for Df(3L)H99.

sli2 Sdcunspecified double heterozygous embryos have additional longitudinal transverse muscles. The number of Fas2-expressing inner fascicles that cross the midline in the double heterozygotes (3.3%) is increased compared to sli2 single heterozygotes (0.6%). Sdcunspecified homozygous embryos that are also heterozygous for sli2 show an enhanced axonal guidance defect with multiple midline crossings of the fascicles.

The combination of heterozygous sli2 and pan-neural overexpression of Rho1N19.Scer\UAS (expressed under the control of Scer\GAL4elav.PLu) leads to longitudinal axon ectopic midline crossing defects. An average of 2 defects are seen per animal, and an average of 18% of segments have defects. If expression of Rho1N19.Scer\UAS is driven by Scer\GAL4ftz.ng, 7.4 defects are seen per animal, and an average of 67% of segments have defects. The combination of heterozygous sli2 and pan-neural overexpression of Rac1N17.Scer\UAS (expressed under the control of Scer\GAL4elav.PLu) leads to longitudinal axon ectopic midline crossing defects. An average of 8.3 defects are seen per animal, and an average of 75% of segments have defects. If expression of Rac1N17.Scer\UAS is driven by Scer\GAL4ftz.ng 4 defects are seen per animal, and an average of 36% of segments have defects. The combination of heterozygous sli2 and pan-neural overexpression of Cdc42N17.Scer\UAS (expressed under the control of Scer\GAL4elav.PLu) does not cause longitudinal axon ectopic midline crossing defects. The combination of heterozygous sli2 and pan-neural overexpression of PakScer\UAS.T:Myr1 under the control of Scer\GAL4elav.PLu leads to longitudinal axon ectopic midline crossing defects. An average of 5.6 defects are seen per animal, and an average of 51% of segments have defects. The combination of heterozygous sli2 and pan-neural overexpression of PakScer\UAS.T:Hsap\MYC under the control of Scer\GAL4elav.PLu leads to longitudinal axon ectopic midline crossing defects. An average of 1.2 defects are seen per animal, and an average of 11% of segments have defects. Co-expression of PakScer\UAS.T:Myr1 partially suppresses longitudinal axon ectopic midline crossing defects seen in sli2/+, Rac1N17.Scer\UAS ; Scer\GAL4elav.PLu animals. An average of 5 defects are seen per animal, and an average of 45% of segments have defects. The combination of heterozygous sli2 and Rac1J11 leads to an enhancement of the longitudinal axon ectopic midline crossing defects. An average of 4.8 defects are seen per animal, and an average of 44% of segments have defects. The combination of heterozygous sli2 and Rac2Δ leads to longitudinal axon ectopic midline crossing defects. An average of 1.4 defects are seen per animal, and an average of 13% of segments have defects. The combination of heterozygous sli2 and MtlΔ leads to longitudinal axon ectopic midline crossing defects. An average of 1.4 defects are seen per animal, and an average of 13% of segments have defects.

sli2/+ robo4/+ double heterozygotes have lch5 and lesA/ldaA axons misprojecting to the v'ch1 pathway in some hemisegments. No stalling of lch5 axons is seen and dorsal sensory axons have a normal morphology.

The ch neurons in sli2/+ robo31/+ embryos frequently show abnormal projections.

98% of lolaORE120 sli2/lolaORE120 embryos show Fas2-expressing axons crossing the midline. There are an average of 4.8 crossovers per affected embryo.

sli2 robounspecified double mutants exhibit midline guidance errors in 44% of embryonic segments (as assayed with Fas2). Embryos with a single copy of sli2 and dock04723 have midline guidance errors in 77% of embryonic segments, sometimes involving all axon fascicles (as assayed with Fas2). In mys1/+ sli2/+ double heterozygous mutants the frequency of midline guidance errors is increased over the level observed in mys1 homozygous mutants. Apart from midline axon crossings in one-third of the segments, the longitudinal tracts (as visible with Fas2) appear normal. In mewM6/+ sli2/+ double heterozygous mutants the frequency of midline guidance errors is increased over the level observed in mewM6 homozygous mutants. Less than 10% of segments revealed midline guidance errors in mewM6/+ sli2/+ embryos.

The frequency of ectopic crossing of the midline by axons in the central nervous system seen in sli2 heterozygous embryos is increased if they are also heterozygous for captB99, captk01217, capt10 or Abl2.

Percentage of segments with midline crossovers in robo1/sli2 transheterozygotes is 45%.

When sli2/sli2 is in combination with unc-5Scer\UAS.T:Ivir\HA1,T:wg, Scer\GAL4elav.PLu the interaction is difficult to interpret - collapse of longitudinal fibers onto the midline is hindered, but midline cells are still displaced.

6% of segments show crossing of the midline by muscles 6/7, 8% show abnormal insertion of muscle 5 and 11% show abnormal insertion of muscles 6/7 in sli2 robo1 double mutant embryos. 1% of segments show crossing of the midline by muscles 6/7, 5% show abnormal insertion of muscle 5 and 3% show abnormal insertion of muscles 6/7 in sli2 leaX123 double mutant embryos. 15% of segments show crossing of the midline by muscles 6/7, 31% show abnormal insertion of muscle 5 and 16% show abnormal insertion of muscles 6/7 in sli2 robo1 leaX123 triple mutant embryos.

The lateral transverse muscles make normal attachments in 98% of segments in embryos expressing roboScer\UAS.cKa under the control of Scer\GAL4how-24B that are also mutant for sli2.

The penetrance of the midline crossover phenotype of Fas2-positive axons in heterozygous embryos is enhanced by one copy of Sose49.

The addition of leaEP2582 (driven by Scer\GAL4elav.PLu) to homozygous sli2 embryos has no effect on the embryonic ventral nerve cord phenotype seen in these embryos.

The Ptp10D1; Ptp69D1/Ptp69D8ex25 double mutant phenotype is significantly enhanced by one copy of sli2; more Fas2-positive axons cross the midline, the longitudinal tracts move closer together and more extensive commissural fusion is seen.

Embryos heterozygous for both robo1 and sli2 show deviation of longitudinal fascicles towards the midline in 74% of segments.

36% of segments contain Fas2-positive neurons inappropriately crossing the midline in sli2/robo1 double heterozygous embryos, in contrast to either single heterozygote which show defects in 1 or 0% of segments. 39% of segments contain Fas2-positive neurons inappropriately crossing the midline in sli2/robo4 double heterozygous embryos, in contrast to either single heterozygote which show defects in 1% of segments.

Dominantly suppresses the wing blister phenotype of if3 flies.

Xenogenetic Interactions
Statement
Reference

Fas2-positive axon bundles cross the midline in 100% of sli2/+ embryos which are also expressing Ggal\MLCKct.Scer\UAS under the control of Scer\GAL4ftz.ng.

The penetrance of the Fas2-positive axon crossover phenotype is increased in sli2 embryos that also carry Khc::Ggal\MLCKKA.ftz compared to either single mutant alone.

Complementation and Rescue Data
Not rescued by
Comments

The sli2 homozygous embryonic heart cardioblast defects (i.e. migration velocity and in filopodial and lamellopodial extensions and activities) and embryonic heart lumen formation defects are partially rescued by the expression of sliScer\UAS.cUa under the control of Scer\GAL4Mef2.247.

Expression of either sliScer\UAS.cBa or sliΔL1-L4.Scer\UAS under the control of Scer\GAL4B2-3-30 leads to a significant recovey in heart cell morphology.

Expression of sliScer\UAS.cKa under the control of Scer\GAL4Mef2.PR (which drives expression in all cardioblasts and somatic muscle cells before they begin their migration toward the dorsal midline) significantly rescues the sli2 mutant phenotype in 95% of cases. The cardioblasts adhere to each other and there are no visible gaps between adjacent cardioblasts and pericardial cells. Rescued embryos show a similar number of of Mef2-positive cardioblasts at the dorsal midline and columnar-shaped cardioblasts similar to wild type controls.

The midline is rescued in sli2 embryos expressing sliScer\UAS.cKa under the control of Scer\GAL4sim.P3.7.

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Mutant
Wild-type
Stocks (2)
Notes on Origin
Discoverer
Comments
Comments

Protein null.

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Synonyms and Secondary IDs (7)
References (78)