Allele Dmel\sli²

General Information
Symbol	Dmel\sli²	Species	D. melanogaster
Name		FlyBase ID	FBal0015700
Feature type	allele	Associated gene	Dmel\sli
Also Known As	slit², sli^IG107, slit^IG107

Map ( GBrowse )
Allele class	loss of function allele, amorphic allele - genetic evidence
Mutagen	ethyl methanesulfonate
Recent Updates
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FB2013_03
FB2013_02
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Nature of the Allele
Allele class	amorphic allele - genetic evidence (Nambu et al., 1990, Klambt et al., 1991, Jacobs, 1993, Battye et al., 1999) loss of function allele (Sonnenfeld and Jacob, 1994, Battye et al., 2001, Simionato et al., 2007, Santiago-Martinez et al., 2006)
Mutagen	ethyl methanesulfonate (Tearle and Nusslein-Volhard, 1987, Nambu et al., 1990, Kolodziej et al., 1995)
Mutations Mapped to the Genome

Type Location Additional Notes References point mutation 2R:11,763,000..11,763,000 evidence=experimental na_change=A11763000T pr_change=K1024\|sli-PA,K1048\|sli-PC,K1024\|sli-PB,K102 4\|sli-PD,K1048@\|sli-PE reported_na_change=A3150T reported_pr_change=K?@ (Battye et al., 2001)
Associated Sequence Data
DDBJ / EMBL / GenBank	DNA sequence Protein sequence Name

UniProtKB/Swiss-Prot
UniProtKB/TrEMBL

Progenitor genotype
Nature of the lesion	Statement Reference Amino acid replacement: K?@. Nucleotide substitution: A3150T. (Battye et al., 2001)
Cytology
Phenotypic Data
Phenotypic Class
	cell polarity defective \| recessive (Qian et al., 2005) cell shape defective \| recessive (Santiago-Martinez et al., 2006) lethal \| recessive (Nambu et al., 1990, Battye et al., 2001) neuroanatomy defective (Keleman and Dickson, 2001, Parsons et al., 2003, Orgogozo et al., 2004, Stevens and Jacobs, 2002, Wills et al., 2002, Kraut and Zinn, 2004, Steigemann et al., 2004, Simionato et al., 2007) neuroanatomy defective (with sli^k04807b) (Tayler et al., 2004) neuroanatomy defective \| dominant (Kim et al., 2002, Garbe et al., 2007) neuroanatomy defective \| dominant \| embryonic stage 16 (Coleman et al., 2010) neuroanatomy defective \| embryonic stage (Lee et al., 2007)
Phenotype Manifest In
	A1-7 dorsal acute muscle 1, with Scer\GAL4^en-e16E, sli^Scer\UAS.cKa (Kramer et al., 2001) A1-7 dorsal acute muscle 1, with Scer\GAL4^sim.P3.7, sli^Scer\UAS.cKa (Kramer et al., 2001) A1-7 dorsal acute muscle 2, with Scer\GAL4^en-e16E, sli^Scer\UAS.cKa (Kramer et al., 2001) A1-7 dorsal acute muscle 2, with Scer\GAL4^sim.P3.7, sli^Scer\UAS.cKa (Kramer et al., 2001) A1-7 dorsal oblique muscle 1, with Scer\GAL4^en-e16E, sli^Scer\UAS.cKa (Kramer et al., 2001) A1-7 dorsal oblique muscle 1, with Scer\GAL4^sim.P3.7, sli^Scer\UAS.cKa (Kramer et al., 2001) A1-7 lateral longitudinal muscle 1, with Scer\GAL4^how-24B, sli^Scer\UAS.cKa (Kramer et al., 2001) A1-7 lateral oblique muscle 1 (Kramer et al., 2001) A1-7 lateral oblique muscle 1, with Scer\GAL4^how-24B, sli^Scer\UAS.cKa (Kramer et al., 2001) A1-7 lateral oblique muscle 1, with Scer\GAL4^sim.P3.7, sli^Scer\UAS.cKa (Kramer et al., 2001) A1-7 ventral longitudinal muscle 2 (Kramer et al., 2001) A1-7 ventral longitudinal muscle 3 (Kramer et al., 2001) A1-7 ventral longitudinal muscle 3, with Scer\GAL4^how-24B, sli^Scer\UAS.cKa (Kramer et al., 2001) A1-7 ventral longitudinal muscle 3, with Scer\GAL4^sim.P3.7, sli^Scer\UAS.cKa (Kramer et al., 2001) A1-7 ventral longitudinal muscle 4 (Kramer et al., 2001) A1-7 ventral longitudinal muscle 4, with Scer\GAL4^how-24B, sli^Scer\UAS.cKa (Kramer et al., 2001) A1-7 ventral longitudinal muscle 4, with Scer\GAL4^sim.P3.7, sli^Scer\UAS.cKa (Kramer et al., 2001) A2-7 dorsal oblique muscle 2, with Scer\GAL4^en-e16E, sli^Scer\UAS.cKa (Kramer et al., 2001) A2-7 dorsal oblique muscle 2, with Scer\GAL4^sim.P3.7, sli^Scer\UAS.cKa (Kramer et al., 2001) abdominal 1 dorsal VUM motor neuron (Klambt et al., 1991) abdominal 1 lateral VUM motor neuron (Klambt et al., 1991) abdominal 1 ventral VUM motor neuron (Klambt et al., 1991) abdominal 2 dorsal VUM motor neuron (Klambt et al., 1991) abdominal 2 lateral VUM motor neuron (Klambt et al., 1991) abdominal 2 ventral VUM motor neuron (Klambt et al., 1991) abdominal 3 dorsal VUM motor neuron (Klambt et al., 1991) abdominal 3 lateral VUM motor neuron (Klambt et al., 1991) abdominal 3 ventral VUM motor neuron (Klambt et al., 1991) abdominal 4 dorsal VUM motor neuron (Klambt et al., 1991) abdominal 4 lateral VUM motor neuron (Klambt et al., 1991) abdominal 4 ventral VUM motor neuron (Klambt et al., 1991) abdominal 5 dorsal VUM motor neuron (Klambt et al., 1991) abdominal 5 lateral VUM motor neuron (Klambt et al., 1991) abdominal 5 ventral VUM motor neuron (Klambt et al., 1991) abdominal 6 dorsal VUM motor neuron (Klambt et al., 1991) abdominal 6 lateral VUM motor neuron (Klambt et al., 1991) abdominal 6 ventral VUM motor neuron (Klambt et al., 1991) abdominal 7 dorsal VUM motor neuron (Klambt et al., 1991) abdominal 7 lateral VUM motor neuron (Klambt et al., 1991) abdominal 7 ventral VUM motor neuron (Klambt et al., 1991) abdominal ventral multidendritic neuron (Orgogozo et al., 2004) aCC neuron (Mehta and Bhat, 2001, Kidd et al., 1999) anterior commissure (Klambt et al., 1991, Battye et al., 2001) axon (Battye et al., 1999) axon & pCC neuron (Lee et al., 2007) cardioblast (Qian et al., 2005, Santiago-Martinez et al., 2006) central nervous system (Battye et al., 1999) chordotonal organ & axon \| lateral (Kolodziej et al., 1995) chordotonal organ & embryo & nerve terminal (Zlatic et al., 2003) class IV dendritic arborizing neuron (Dimitrova et al., 2008) commissure (Battye et al., 1999, Simionato et al., 2007) dendrite (Dimitrova et al., 2008) dorsal abdominal cluster (Dimitrova et al., 2008) dorsal neurohemal organ (Zhou et al., 1997) embryonic/larval neuron (Garbe et al., 2007) embryonic/larval somatic muscle \| ectopic, with Scer\GAL4^sim.P3.7, sli^Scer\UAS.cKa (Kramer et al., 2001) embryonic/larval somatic muscle \| ventral (Kramer et al., 2001) embryonic pericardial cell (Santiago-Martinez et al., 2006) embryonic somatic muscle \| ventral (Steigemann et al., 2004) eye photoreceptor cell & axon (with sli^k04807b) (Tayler et al., 2004) fascicle (Stevens and Jacobs, 2002) ganglion mother cell GMC1-1a (Mehta and Bhat, 2001) germline cell \| embryonic stage (with Df(2R)Jp5) (Weyers et al., 2011) gonad \| embryonic stage (with Df(2R)Jp5) (Weyers et al., 2011) gonadal sheath proper primordium \| embryonic stage (with Df(2R)Jp5) (Weyers et al., 2011) heart primordium (Qian et al., 2005, MacMullin and Jacobs, 2006) intermediate longitudinal fascicle (Zlatic et al., 2003) lamina anlage (with sli^k04807b) (Tayler et al., 2004) lamina anlage glial cell (with sli^k04807b) (Tayler et al., 2004) lamina neuropil (with sli^k04807b) (Tayler et al., 2004) lateral longitudinal fascicle (Zlatic et al., 2003) lateral multidendritic neuron ldaA (Parsons et al., 2003) lch5 neuron (Parsons et al., 2003) lesA neuron (Parsons et al., 2003) longitudinal connective (Nambu et al., 1990, Fritz and VanBerkum, 2000, Klambt et al., 1991, Sonnenfeld and Jacob, 1994, Keleman and Dickson, 2001, Battye et al., 2001, Kim et al., 2002, Battye et al., 1999) longitudinal connective \| embryonic stage 16 (Coleman et al., 2010) medial longitudinal fascicle (Zlatic et al., 2003) mesectoderm (Battye et al., 1999) mesothoracic dorsal triscolopidial chordotonal organ dch3 (Kraut and Zinn, 2004) mesothoracic dorsal triscolopidial chordotonal organ dch3 & scolopidial dendrite (Kraut and Zinn, 2004) metathoracic dorsal triscolopidial chordotonal organ dch3 (Kraut and Zinn, 2004) metathoracic dorsal triscolopidial chordotonal organ dch3 & scolopidial dendrite (Kraut and Zinn, 2004) midline crossing tract \| embryonic stage 16 (Coleman et al., 2010) midline glial cell (Klambt et al., 1991, Sonnenfeld and Jacob, 1994, Battye et al., 1999) motor neuron (Parsons et al., 2003) MP1 neuron (Klambt et al., 1991, Sonnenfeld and Jacob, 1994, Battye et al., 1999) muscle attachment site \| ectopic (Deng et al., 2010) neuroblast MNB (Klambt et al., 1991) pCC neuron (Kidd et al., 1999) posterior commissure (Klambt et al., 1991, Battye et al., 2001) presumptive embryonic/larval central nervous system (Kidd et al., 1999, Wills et al., 2002, Sun et al., 2000, Steigemann et al., 2004) presumptive embryonic/larval muscle system (Kidd et al., 1999) presumptive embryonic salivary gland (Kolesnikov and Beckendorf, 2005) RP2 motor neuron (Mehta and Bhat, 2001) RP2 motor neuron \| ectopic (Mehta and Bhat, 2001) RP2sib neuron (Mehta and Bhat, 2001) SP1 neuron (Kidd et al., 1999) spiracular branch primordium (Parsons et al., 2003) transverse connective primordium (Parsons et al., 2003) ventral longitudinal muscle (Deng et al., 2010) ventral midline (Kramer et al., 2001) ventral nerve cord (Battye et al., 2001) ventral nervous system (Battye et al., 1999) ventral oblique muscle (Battye et al., 2001, Battye et al., 1999) vMP2 neuron (Battye et al., 1999) VUM interneuron 1 (Sonnenfeld and Jacob, 1994) VUM interneuron 2 (Sonnenfeld and Jacob, 1994) VUM interneuron 3 (Sonnenfeld and Jacob, 1994) VUM neuron (Sonnenfeld and Jacob, 1994)
Detailed Description
	Statement Reference Tracheal dorsal branch fusion occurs normally in the tracheal system of sli[2]/+ third instar larvae (Schulz et al., 2011) sli[2]/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. (Weyers et al., 2011) Mild ectopic ap neuron crossing defects are seen in heterozygous sli[2] stage 16 embryos. (Coleman et al., 2010) In sli[2] 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. (Deng et al., 2010) Many of the dorsal abdominal clusters in sli[2] 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 sli[2] 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 robo[1] mutants at 22 hours after egg laying. The dorsal elongation and the average branch length are significantly increased. (Dimitrova et al., 2008) 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. (Garbe et al., 2007) In robo² embryos, the pCC axons aberrantly cross the midline. (Lee et al., 2007) sli[2] mutant embryos present a very severe fused commissure phenotype. (Simionato et al., 2007) 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. (MacMullin and Jacobs, 2006) 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. (Santiago-Martinez et al., 2006) 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. (Kolesnikov and Beckendorf, 2005) 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. (Qian et al., 2005) Normal separation of primordial germ cells into lateral clusters on each side of the embryo is observed in homozygous and heterozygous sli². (Sano et al., 2005) 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. (Kraut and Zinn, 2004) 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. (Orgogozo et al., 2004) 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. (Steigemann et al., 2004) sli^k04807b/sli² third instar larvae show defects in photoreceptor axon targeting, with gaps in the lamina and increased numbers of axons entering the medulla. sli^k04807b/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 sli^k04807b/sli² third instar larvae and some distal cell neurons invade the lamina neuropil, disrupting photoreceptor innervation. (Tayler et al., 2004) Heterozygous mutants do not exhibit significant longitudinal axon ectopic midline crossing defects. (Fan et al., 2003) 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. (Parsons et al., 2003) 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. (Zlatic et al., 2003) Heterozygous embryos only extremely rarely show Fas2-expressing axons crossing the midline. (Crowner et al., 2002) One or two Fas2-positive axon bundles cross the midline in about 36% of heterozygous embryos. (Kim et al., 2002) sli² heterozygotes exhibit 3.4% midline errors (as assayed with Fas2). (Stevens and Jacobs, 2002) Heterozygotes show 4% ectopic crossing of the midline by axons in the embryonic central nervous system. (Wills et al., 2002) 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. (Battye et al., 2001) All CNS axons converge on the midline which is displaced ventrally. (Keleman and Dickson, 2001) 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 sli^Scer\UAS.cKa under the control of Scer\GAL4^sim.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. (Kramer et al., 2001) sli² embryos in which the midline has been rescued by expressing sli^Scer\UAS.cKa under the control of Scer\GAL4^sim.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 sli^Scer\UAS.cKa under the control of Scer\GAL4^en-e16E, 49% of segments show muscle cells aligned with sites of ectopic sli expression. In sli² embryos expressing sli^Scer\UAS.cKa under the control of Scer\GAL4^ptc-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. (Kramer et al., 2001) The GMC-1 in mutants frequently (about 10%) divide symmetrically to generate two RP2s instead of an RP2 and a sib. (Mehta and Bhat, 2001) Approximately 24% of heterozygous embryos show periodic crossovers of Fas2-positive axons across the midline. (Fritz and VanBerkum, 2000) All central nervous system axons converge on the midline in sli¹/sli² embryos. (Sun et al., 2000) 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 sli^Scer\UAS.cBa, Scer\GAL4^sim.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. (Battye et al., 1999) 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. (Kidd et al., 1999) 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. (Zhou et al., 1997) Mutant phenotype as assayed by Ecol\lacZ^rp staining: midline missing. Mutant phenotype of lateral chordotonal axons includes: shorter axons, defasciculated axons or dorsally routed axons. (Kolodziej et al., 1995) 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. (Sonnenfeld and Jacob, 1994) Longitudinal tracts fuse at the ventral midline, though the glial scaffold is normal. (Jacobs, 1993) 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. (Klambt et al., 1991) The presence of Ecol\lacZ^sim.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. (Nambu et al., 1990)
External Data
Linkouts
Interactions
	Show the genetic interaction network for Enhancers & Suppressors
Phenotypic Class
Enhanced by
Statement Reference robo[+]/robo¹, sli² has neuroanatomy defective phenotype, enhanceable by β-Spec^em6 (Garbe et al., 2007) robo[+]/robo¹, sli² has neuroanatomy defective phenotype, enhanceable by β-Spec^G0074 (Garbe et al., 2007) robo[+]/robo¹, sli² has neuroanatomy defective phenotype, enhanceable by β-Spec^G0198 (Garbe et al., 2007) shot³/shot[+], sli² has neuroanatomy defective \| embryonic stage phenotype, enhanceable by exba[+]/exba² (Lee et al., 2007) sli² has neuroanatomy defective \| dominant \| embryonic stage 16 phenotype, enhanceable by kuz[+]/kuz¹¹² (Coleman et al., 2010) sli² has neuroanatomy defective \| dominant \| embryonic stage 16 phenotype, enhanceable by kuz[+]/kuz²⁵⁸³ (Coleman et al., 2010) sli² has neuroanatomy defective \| dominant \| embryonic stage 16 phenotype, enhanceable by kuz[+]/kuz^H143 (Coleman et al., 2010) sli² has neuroanatomy defective \| dominant \| embryonic stage 16 phenotype, enhanceable by Scer\GAL4^ap-md544/kuz^DN.Scer\UAS (Coleman et al., 2010) sli² has neuroanatomy defective \| dominant phenotype, enhanceable by β-Spec^em6 (Garbe et al., 2007) sli² has neuroanatomy defective \| dominant phenotype, enhanceable by β-Spec^G0198 (Garbe et al., 2007) sli² has neuroanatomy defective \| embryonic stage phenotype, enhanceable by exba[+]/exba² (Lee et al., 2007) sli² has neuroanatomy defective \| embryonic stage phenotype, enhanceable by shot³/shot[+] (Lee et al., 2007) sli² has neuroanatomy defective phenotype, enhanceable by Abl²/Abl[+] (Wills et al., 2002) sli² has neuroanatomy defective phenotype, enhanceable by capt[+]/capt^B99 (Wills et al., 2002) sli² has neuroanatomy defective phenotype, enhanceable by capt¹⁰/capt[+] (Wills et al., 2002) sli² has neuroanatomy defective phenotype, enhanceable by capt^k01217/capt[+] (Wills et al., 2002) sli² has neuroanatomy defective phenotype, enhanceable by dock⁰⁴⁷²³ (Stevens and Jacobs, 2002) sli² has neuroanatomy defective phenotype, enhanceable by Ggal\MLCK^ct.Scer\UAS/Scer\GAL4^ftz.ng (Kim et al., 2002) sli² has neuroanatomy defective phenotype, enhanceable by robo^unspecified (Stevens and Jacobs, 2002)
NOT Enhanced by
Statement Reference robo¹, sli² has neuroanatomy defective \| embryonic stage 16 phenotype, non-enhanceable by Df(3R)ED4688 (Keleman et al., 2005) robo¹, sli² has neuroanatomy defective \| embryonic stage 16 phenotype, non-enhanceable by Nedd4^EY00500/Scer\GAL4¹⁴⁰⁷ (Keleman et al., 2005) robo¹, sli² has neuroanatomy defective \| embryonic stage 16 phenotype, non-enhanceable by Nedd4^EY00500/Scer\GAL4^elav.PLu (Keleman et al., 2005) robo¹, sli² has neuroanatomy defective \| embryonic stage 16 phenotype, non-enhanceable by Nedd4^{Scer\UAS.T:Hsap\MYC}/Scer\GAL4¹⁴⁰⁷ (Keleman et al., 2005) robo¹, sli² has neuroanatomy defective \| embryonic stage 16 phenotype, non-enhanceable by Nedd4^{Scer\UAS.T:Hsap\MYC}/Scer\GAL4^elav.PLu (Keleman et al., 2005)
Suppressed by
Statement Reference Rac1^N17.Scer\UAS, Scer\GAL4^elav.PLu, sli² has neuroanatomy defective phenotype, suppressible \| partially by Pak^{Scer\UAS.T:Myr-Src64B}, Scer\GAL4^elav.PLu (Fan et al., 2003) robo¹, sli² has neuroanatomy defective \| embryonic stage 16 phenotype, suppressible by ena^Scer\UAS.cCa/Scer\GAL4^elav.PLu (Keleman et al., 2005) sli² has neuroanatomy defective phenotype, suppressible \| partially by elav⁵ (Simionato et al., 2007) β-Spec^em6, robo[+]/robo¹, sli² has neuroanatomy defective phenotype, suppressible \| partially by β-Spec^{Scer\UAS.T:Hsap\MYC}/Scer\GAL4^elav.PLu (Garbe et al., 2007)
NOT suppressed by
Statement Reference sli² has neuroanatomy defective phenotype, non-suppressible by Df(3L)H99 (Orgogozo et al., 2004) β-Spec^em6, sli² has neuroanatomy defective \| dominant phenotype, non-suppressible by Scer\GAL4^ap-md544/β-Spec^{Scer\UAS.T:Hsap\MYC} (Garbe et al., 2007)
Enhancer of
Statement Reference sli², robo[+], robo¹ is an enhancer of neuroanatomy defective phenotype of β-Spec^em6 (Garbe et al., 2007) sli², robo[+], robo¹ is an enhancer of neuroanatomy defective phenotype of β-Spec^G0074 (Garbe et al., 2007) sli², robo[+], robo¹ is an enhancer of neuroanatomy defective phenotype of β-Spec^G0198 (Garbe et al., 2007) sli²/sli[+] is an enhancer of neuroanatomy defective \| dominant \| embryonic stage 16 phenotype of kuz^H143 (Coleman et al., 2010) sli²/sli[+] is an enhancer of neuroanatomy defective \| embryonic stage 16 phenotype of Scer\GAL4^ap-md544, kuz^DN.Scer\UAS (Coleman et al., 2010) sli²/sli[+] is an enhancer of neuroanatomy defective phenotype of comm^unspecified (Bhat et al., 2007) sli²/sli[+] is an enhancer of neuroanatomy defective phenotype of elav⁵ (Simionato et al., 2007) sli²/sli[+] is an enhancer of neuroanatomy defective phenotype of Ggal\MLCK^ct.Scer\UAS, Scer\GAL4^ftz.ng (Kim et al., 2002) sli²/sli[+] is an enhancer of neuroanatomy defective phenotype of lola^ORE120 (Crowner et al., 2002) sli²/sli[+] is an enhancer of neuroanatomy defective phenotype of Sdc^unspecified (Steigemann et al., 2004) sli² is an enhancer of neuroanatomy defective phenotype of dock⁰⁴⁷²³ (Stevens and Jacobs, 2002) sli² is an enhancer of neuroanatomy defective phenotype of if^k27e (Stevens and Jacobs, 2002) sli² is an enhancer of neuroanatomy defective phenotype of mew^M6 (Stevens and Jacobs, 2002) sli² is an enhancer of neuroanatomy defective phenotype of mys¹ (Stevens and Jacobs, 2002) sli² is an enhancer of neuroanatomy defective phenotype of robo^unspecified (Stevens and Jacobs, 2002) sli² is an enhancer of neuroanatomy defective phenotype of scb^unspecified (Stevens and Jacobs, 2002)
NOT Enhancer of
Statement Reference sli²/sli[+] is a non-enhancer of neuroanatomy defective phenotype of egh⁷ (Fan et al., 2005)
Suppressor of
Statement Reference sli²/sli[+] is a suppressor \| partially of neuroanatomy defective phenotype of Scer\GAL4^elav-C155, lea^EP2582 (Kraut and Zinn, 2004) sli²/sli[+] is a suppressor of visible phenotype of if³ (Wessendorf et al., 1992)
NOT Suppressor of
Statement Reference sli²/sli[+] is a non-suppressor of neuroanatomy defective phenotype of egh⁷ (Fan et al., 2005) sli² is a non-suppressor of neuroanatomy defective \| embryonic stage phenotype of Scer\GAL4^elav.PLu, fra^{ΔC.Scer\UAS.T:Ivir\HA1}, fra^unspecified (Garbe et al., 2007)
Other
Statement Reference chb⁴, sli²/sli[+] has neuroanatomy defective phenotype (Lee et al., 2004) chb⁴, sli² has neuroanatomy defective phenotype (Lee et al., 2004) chb^P4, sli²/sli[+] has neuroanatomy defective phenotype (Lee et al., 2004) chb^P4, sli² has neuroanatomy defective phenotype (Lee et al., 2004) LanA^9-32, scb^unspecified, sli² has neuroanatomy defective phenotype (Stevens and Jacobs, 2002) Mtl^Δ, sli² has neuroanatomy defective phenotype (Fan et al., 2003) Pak^{Scer\UAS.T:Hsap\MYC}, Scer\GAL4^elav.PLu, sli² has neuroanatomy defective phenotype (Fan et al., 2003) Pak^{Scer\UAS.T:Myr-Src64B}, Scer\GAL4^elav.PLu, sli² has neuroanatomy defective phenotype (Fan et al., 2003) Rac1^J11, sli² has neuroanatomy defective phenotype (Fan et al., 2003) Rac1^N17.Scer\UAS, Scer\GAL4^elav.PLu, sli² has neuroanatomy defective phenotype (Fan et al., 2003) Rac1^N17.Scer\UAS, Scer\GAL4^ftz.ng, sli² has neuroanatomy defective phenotype (Fan et al., 2003) Rac2^Δ, sli² has neuroanatomy defective phenotype (Fan et al., 2003) Rho1^N19.Scer\UAS, Scer\GAL4^elav.PLu, sli² has neuroanatomy defective phenotype (Fan et al., 2003) Rho1^N19.Scer\UAS, Scer\GAL4^ftz.ng, sli² has neuroanatomy defective phenotype (Fan et al., 2003) robo[+]/robo¹, sli² has neuroanatomy defective phenotype (Garbe et al., 2007) robo[+]/robo⁴, sli² has neuroanatomy defective phenotype (Parsons et al., 2003) robo¹, sli² has neuroanatomy defective \| embryonic stage 16 phenotype (Keleman et al., 2005) robo⁴, sli² has neuroanatomy defective phenotype (Parsons et al., 2003) Sac1¹/Sac1[+], sli² has neuroanatomy defective \| dominant \| embryonic stage phenotype (Lee et al., 2011) Scer\GAL4^elav.PLu, sli², unc-5^{Scer\UAS.T:Ivir\HA1,T:SS-wg} has neuroanatomy defective phenotype (Keleman and Dickson, 2001, Keleman and Dickson, 2001, Keleman and Dickson, 2001) Sdc[+]/Sdc^unspecified, sli² has neuroanatomy defective phenotype (Steigemann et al., 2004) Sdc^unspecified, sli² has neuroanatomy defective phenotype (Steigemann et al., 2004)
Phenotype Manifest In
Enhanced by
Statement Reference robo[+]/robo¹, sli² has medial longitudinal fascicle \| ectopic phenotype, enhanceable by β-Spec^em6 (Garbe et al., 2007) robo[+]/robo¹, sli² has medial longitudinal fascicle \| ectopic phenotype, enhanceable by β-Spec^G0074 (Garbe et al., 2007) robo[+]/robo¹, sli² has medial longitudinal fascicle \| ectopic phenotype, enhanceable by β-Spec^G0198 (Garbe et al., 2007) shot³/shot[+], sli² has axon & pCC neuron phenotype, enhanceable by exba[+]/exba² (Lee et al., 2007) sli² has axon & pCC neuron phenotype, enhanceable by exba[+]/exba² (Lee et al., 2007) sli² has axon & pCC neuron phenotype, enhanceable by shot³/shot[+] (Lee et al., 2007) sli² has embryonic/larval neuron phenotype, enhanceable by β-Spec^em6 (Garbe et al., 2007) sli² has embryonic/larval neuron phenotype, enhanceable by β-Spec^G0198 (Garbe et al., 2007) sli² has fascicle phenotype, enhanceable by dock⁰⁴⁷²³ (Stevens and Jacobs, 2002) sli² has fascicle phenotype, enhanceable by robo^unspecified (Stevens and Jacobs, 2002) sli² has heart primordium phenotype, enhanceable by Ilk[+]/Ilk^ZCL3111 (MacMullin and Jacobs, 2006) sli² has heart primordium phenotype, enhanceable by LanA^9-32/LanA[+] (MacMullin and Jacobs, 2006) sli² has heart primordium phenotype, enhanceable by lea[+]/lea² (MacMullin and Jacobs, 2006) sli² has heart primordium phenotype, enhanceable by lea[+]/lea^S4-18 (MacMullin and Jacobs, 2006) sli² has heart primordium phenotype, enhanceable by mys¹/mys[+] (MacMullin and Jacobs, 2006) sli² has heart primordium phenotype, enhanceable by Nrt[+]/Nrt^M54 (MacMullin and Jacobs, 2006) sli² has heart primordium phenotype, enhanceable by Ras85D⁰⁵⁷⁰³/Ras85D[+] (MacMullin and Jacobs, 2006) sli² has heart primordium phenotype, enhanceable by rhea[+]/rhea¹ (MacMullin and Jacobs, 2006) sli² has heart primordium phenotype, enhanceable by scb[+]/scb⁰¹²⁸⁸ (MacMullin and Jacobs, 2006) sli² has heart primordium phenotype, enhanceable by vkg[+]/vkg^P10038 (MacMullin and Jacobs, 2006) sli² has heart primordium phenotype, enhanceable by vkg¹⁷⁷/vkg[+] (MacMullin and Jacobs, 2006) sli² has heart primordium phenotype, enhanceable by wb[+]/wb^SF11 (MacMullin and Jacobs, 2006) sli² has longitudinal connective \| embryonic stage 16 phenotype, enhanceable by kuz[+]/kuz¹¹² (Coleman et al., 2010) sli² has longitudinal connective \| embryonic stage 16 phenotype, enhanceable by kuz[+]/kuz²⁵⁸³ (Coleman et al., 2010) sli² has longitudinal connective \| embryonic stage 16 phenotype, enhanceable by kuz[+]/kuz^H143 (Coleman et al., 2010) sli² has longitudinal connective \| embryonic stage 16 phenotype, enhanceable by Scer\GAL4^ap-md544/kuz^DN.Scer\UAS (Coleman et al., 2010) sli² has longitudinal connective phenotype, enhanceable by Ggal\MLCK^ct.Scer\UAS/Scer\GAL4^ftz.ng (Kim et al., 2002) sli² has longitudinal connective phenotype, enhanceable by Khc::Ggal\MLCK^KA.ftz (Fritz and VanBerkum, 2000) sli² has longitudinal connective phenotype, enhanceable by robo[+]/robo¹ (Battye et al., 1999) sli² has longitudinal connective phenotype, enhanceable by Sos^e49 (Fritz and VanBerkum, 2000) sli² has midline crossing tract \| embryonic stage 16 phenotype, enhanceable by kuz[+]/kuz¹¹² (Coleman et al., 2010) sli² has midline crossing tract \| embryonic stage 16 phenotype, enhanceable by kuz[+]/kuz²⁵⁸³ (Coleman et al., 2010) sli² has midline crossing tract \| embryonic stage 16 phenotype, enhanceable by kuz[+]/kuz^H143 (Coleman et al., 2010) sli² has midline crossing tract \| embryonic stage 16 phenotype, enhanceable by Scer\GAL4^ap-md544/kuz^DN.Scer\UAS (Coleman et al., 2010) sli² has muscle attachment site \| ectopic phenotype, enhanceable by vg^2.Scer\UAS/Scer\GAL4^Mef2.PR (Deng et al., 2010) sli² has muscle attachment site phenotype, enhanceable by vg^2.Scer\UAS/Scer\GAL4^Mef2.PR (Deng et al., 2010) sli² has presumptive embryonic/larval central nervous system phenotype, enhanceable by Abl²/Abl[+] (Wills et al., 2002) sli² has presumptive embryonic/larval central nervous system phenotype, enhanceable by capt[+]/capt^B99 (Wills et al., 2002) sli² has presumptive embryonic/larval central nervous system phenotype, enhanceable by capt¹⁰/capt[+] (Wills et al., 2002) sli² has presumptive embryonic/larval central nervous system phenotype, enhanceable by capt^k01217/capt[+] (Wills et al., 2002) sli² has presumptive embryonic/larval central nervous system phenotype, enhanceable by Sdc[+]/Sdc^unspecified (Steigemann et al., 2004) sli² has ventral nerve cord phenotype, enhanceable by robo[+]/robo¹ (Battye et al., 2001)
NOT Enhanced by
Statement Reference robo¹, sli² has longitudinal connective \| embryonic stage 16 phenotype, non-enhanceable by Df(3R)ED4688 (Keleman et al., 2005) robo¹, sli² has longitudinal connective \| embryonic stage 16 phenotype, non-enhanceable by Nedd4^EY00500/Scer\GAL4¹⁴⁰⁷ (Keleman et al., 2005) robo¹, sli² has longitudinal connective \| embryonic stage 16 phenotype, non-enhanceable by Nedd4^EY00500/Scer\GAL4^elav.PLu (Keleman et al., 2005) robo¹, sli² has longitudinal connective \| embryonic stage 16 phenotype, non-enhanceable by Nedd4^{Scer\UAS.T:Hsap\MYC}/Scer\GAL4¹⁴⁰⁷ (Keleman et al., 2005) robo¹, sli² has longitudinal connective \| embryonic stage 16 phenotype, non-enhanceable by Nedd4^{Scer\UAS.T:Hsap\MYC}/Scer\GAL4^elav.PLu (Keleman et al., 2005) robo¹, sli² has midline crossing tract \| embryonic stage 16 phenotype, non-enhanceable by Df(3R)ED4688 (Keleman et al., 2005) robo¹, sli² has midline crossing tract \| embryonic stage 16 phenotype, non-enhanceable by Nedd4^EY00500/Scer\GAL4¹⁴⁰⁷ (Keleman et al., 2005) robo¹, sli² has midline crossing tract \| embryonic stage 16 phenotype, non-enhanceable by Nedd4^EY00500/Scer\GAL4^elav.PLu (Keleman et al., 2005) robo¹, sli² has midline crossing tract \| embryonic stage 16 phenotype, non-enhanceable by Nedd4^{Scer\UAS.T:Hsap\MYC}/Scer\GAL4¹⁴⁰⁷ (Keleman et al., 2005) robo¹, sli² has midline crossing tract \| embryonic stage 16 phenotype, non-enhanceable by Nedd4^{Scer\UAS.T:Hsap\MYC}/Scer\GAL4^elav.PLu (Keleman et al., 2005) sli² has heart primordium phenotype, non-enhanceable by dock[+]/dock⁰⁴⁷²³ (MacMullin and Jacobs, 2006) sli² has heart primordium phenotype, non-enhanceable by mew[+]/mew^M6 (MacMullin and Jacobs, 2006) sli² has heart primordium phenotype, non-enhanceable by Tig^x/Tig[+] (MacMullin and Jacobs, 2006)
Suppressed by
Statement Reference Rac1^N17.Scer\UAS, Scer\GAL4^elav.PLu, sli² has longitudinal connective phenotype, suppressible \| partially by Pak^{Scer\UAS.T:Myr-Src64B}, Scer\GAL4^elav.PLu (Fan et al., 2003) robo¹, sli² has longitudinal connective \| embryonic stage 16 phenotype, suppressible by ena^Scer\UAS.cCa/Scer\GAL4^elav.PLu (Keleman et al., 2005) robo¹, sli² has midline crossing tract \| embryonic stage 16 phenotype, suppressible by ena^Scer\UAS.cCa/Scer\GAL4^elav.PLu (Keleman et al., 2005) sli² has muscle attachment site \| ectopic phenotype, suppressible by Scer\GAL4^Mef2.PR/Egfr^DN.Scer\UAS (Deng et al., 2010) sli² has muscle attachment site \| ectopic phenotype, suppressible by sd^{Δ88-159.Scer\UAS}/Scer\GAL4^Mef2.PR (Deng et al., 2010) sli² has muscle attachment site phenotype, suppressible by Scer\GAL4^Mef2.PR/Egfr^DN.Scer\UAS (Deng et al., 2010) sli² has muscle attachment site phenotype, suppressible by sd^{Δ88-159.Scer\UAS}/Scer\GAL4^Mef2.PR (Deng et al., 2010) sli² has presumptive embryonic salivary gland phenotype, suppressible by fra³/fra⁴ (Kolesnikov and Beckendorf, 2005) β-Spec^em6, robo[+]/robo¹, sli² has medial longitudinal fascicle \| ectopic phenotype, suppressible \| partially by β-Spec^{Scer\UAS.T:Hsap\MYC}/Scer\GAL4^elav.PLu (Garbe et al., 2007)
NOT suppressed by
Statement Reference sli² has abdominal ventral multidendritic neuron phenotype, non-suppressible by Df(3L)H99 (Orgogozo et al., 2004) sli² has ventral nerve cord phenotype, non-suppressible by lea^EP2582/Scer\GAL4^elav.PLu (Rajagopalan et al., 2000) β-Spec^em6, sli² has embryonic/larval neuron phenotype, non-suppressible by Scer\GAL4^ap-md544/β-Spec^{Scer\UAS.T:Hsap\MYC} (Garbe et al., 2007)
Enhancer of
Statement Reference sli², robo[+], robo¹ is an enhancer of medial longitudinal fascicle \| ectopic phenotype of β-Spec^em6 (Garbe et al., 2007) sli², robo[+], robo¹ is an enhancer of medial longitudinal fascicle \| ectopic phenotype of β-Spec^G0074 (Garbe et al., 2007) sli², robo[+], robo¹ is an enhancer of medial longitudinal fascicle \| ectopic phenotype of β-Spec^G0198 (Garbe et al., 2007) sli², Scer\GAL4^ap-md544, sli[+] is an enhancer of longitudinal connective \| embryonic stage 16 phenotype of Scer\GAL4^ap-md544, kuz^DN.Scer\UAS (Coleman et al., 2010) sli², Scer\GAL4^ap-md544, sli[+] is an enhancer of midline crossing tract \| embryonic stage 16 phenotype of Scer\GAL4^ap-md544, kuz^DN.Scer\UAS (Coleman et al., 2010) sli²/LanA^9-32 is an enhancer of fascicle phenotype of scb^unspecified (Stevens and Jacobs, 2002) sli²/sli[+] is an enhancer of chordotonal organ & embryo & nerve terminal phenotype of robo3¹ (Zlatic et al., 2003) sli²/sli[+] is an enhancer of commissure phenotype of elav⁵ (Simionato et al., 2007) sli²/sli[+] is an enhancer of dorsal closure embryo phenotype of scb⁰¹²⁸⁸ (MacMullin and Jacobs, 2006) sli²/sli[+] is an enhancer of longitudinal connective \| embryonic stage 16 phenotype of kuz^H143 (Coleman et al., 2010) sli²/sli[+] is an enhancer of longitudinal connective phenotype of Abl^EP3101, Scer\GAL4^elav.PLu (Bashaw et al., 2000) sli²/sli[+] is an enhancer of longitudinal connective phenotype of comm^unspecified (Bhat et al., 2007) sli²/sli[+] is an enhancer of longitudinal connective phenotype of Ggal\MLCK^ct.Scer\UAS, Scer\GAL4^ftz.ng (Kim et al., 2002) sli²/sli[+] is an enhancer of longitudinal connective phenotype of lola^ORE120 (Crowner et al., 2002) sli²/sli[+] is an enhancer of longitudinal connective phenotype of Ptp10D¹, Ptp69D¹/Ptp69D^8ex25 (Sun et al., 2000) sli²/sli[+] is an enhancer of longitudinal connective phenotype of robo¹ (Battye et al., 1999) sli²/sli[+] is an enhancer of midline crossing tract \| embryonic stage 16 phenotype of kuz^H143 (Coleman et al., 2010) sli²/sli[+] is an enhancer of presumptive embryonic/larval central nervous system phenotype of Ptp10D¹, Ptp69D¹/Ptp69D^8ex25 (Sun et al., 2000) sli²/sli[+] is an enhancer of presumptive embryonic/larval central nervous system phenotype of Sdc^unspecified (Steigemann et al., 2004) sli²/sli[+] is an enhancer of ventral nerve cord commissure phenotype of Ptp10D¹, Ptp69D¹/Ptp69D^8ex25 (Sun et al., 2000) sli² is an enhancer of fascicle phenotype of dock⁰⁴⁷²³ (Stevens and Jacobs, 2002) sli² is an enhancer of fascicle phenotype of mew^M6 (Stevens and Jacobs, 2002) sli² is an enhancer of fascicle phenotype of mys¹ (Stevens and Jacobs, 2002) sli² is an enhancer of fascicle phenotype of robo^unspecified (Stevens and Jacobs, 2002) sli² is an enhancer of fascicle phenotype of scb^unspecified (Stevens and Jacobs, 2002) sli² is an enhancer of longitudinal connective phenotype of Khc::Ggal\MLCK^KA.ftz (Fritz and VanBerkum, 2000)
NOT Enhancer of
Statement Reference sli²/sli[+] is a non-enhancer of photoreceptor cell R1 & axon phenotype of egh⁷ (Fan et al., 2005) sli²/sli[+] is a non-enhancer of photoreceptor cell R2 & axon phenotype of egh⁷ (Fan et al., 2005) sli²/sli[+] is a non-enhancer of photoreceptor cell R3 & axon phenotype of egh⁷ (Fan et al., 2005) sli²/sli[+] is a non-enhancer of photoreceptor cell R4 & axon phenotype of egh⁷ (Fan et al., 2005) sli²/sli[+] is a non-enhancer of photoreceptor cell R5 & axon phenotype of egh⁷ (Fan et al., 2005) sli²/sli[+] is a non-enhancer of photoreceptor cell R6 & axon phenotype of egh⁷ (Fan et al., 2005)
Suppressor of
Statement Reference sli²/sli[+] is a suppressor \| partially of abdominal lateral pentascolopidial chordotonal organ lch5 phenotype of Scer\GAL4^elav-C155, lea^EP2582 (Kraut and Zinn, 2004) sli²/sli[+] is a suppressor \| partially of dorsal branch \| third instar larval stage phenotype of Sdc²⁶³⁹ (Schulz et al., 2011) sli²/sli[+] is a suppressor of dorsal branch \| third instar larval stage phenotype of Scer\GAL4^btl.PS, Sdc^{dsRNA.Scer\UAS.cSa} (Schulz et al., 2011) sli²/sli[+] is a suppressor of wing phenotype of if³ (Wessendorf et al., 1992) sli² is a suppressor \| partially of ventral nerve cord commissure phenotype of Scer\GAL4^elav.PLu, lea^Scer\UAS.cSa (Simpson et al., 2000) sli² is a suppressor of A1-7 lateral transverse muscle 1 phenotype of Scer\GAL4^how-24B/Scer\GAL4^how-24B, robo^Scer\UAS.cKa (Kramer et al., 2001) sli² is a suppressor of A1-7 lateral transverse muscle 2 phenotype of Scer\GAL4^how-24B/Scer\GAL4^how-24B, robo^Scer\UAS.cKa (Kramer et al., 2001) sli² is a suppressor of A1-7 lateral transverse muscle 3 phenotype of Scer\GAL4^how-24B/Scer\GAL4^how-24B, robo^Scer\UAS.cKa (Kramer et al., 2001)
NOT Suppressor of
Statement Reference sli²/sli[+] is a non-suppressor of photoreceptor cell R1 & axon phenotype of egh⁷ (Fan et al., 2005) sli²/sli[+] is a non-suppressor of photoreceptor cell R2 & axon phenotype of egh⁷ (Fan et al., 2005) sli²/sli[+] is a non-suppressor of photoreceptor cell R3 & axon phenotype of egh⁷ (Fan et al., 2005) sli²/sli[+] is a non-suppressor of photoreceptor cell R4 & axon phenotype of egh⁷ (Fan et al., 2005) sli²/sli[+] is a non-suppressor of photoreceptor cell R5 & axon phenotype of egh⁷ (Fan et al., 2005) sli²/sli[+] is a non-suppressor of photoreceptor cell R6 & axon phenotype of egh⁷ (Fan et al., 2005) sli² is a non-suppressor of ventral nerve cord commissure \| embryonic stage phenotype of Scer\GAL4^elav.PLu, fra^{ΔC.Scer\UAS.T:Ivir\HA1}, fra^unspecified (Garbe et al., 2007)
Other
Statement Reference +/Df(2R)Jp6, sli² has cardioblast phenotype (Qian et al., 2005) chb⁴, sli²/sli[+] has embryonic/larval neuron phenotype (Lee et al., 2004) chb⁴, sli² has embryonic/larval neuron phenotype (Lee et al., 2004) chb^P4, sli²/sli[+] has embryonic/larval neuron phenotype (Lee et al., 2004) chb^P4, sli² has embryonic/larval neuron phenotype (Lee et al., 2004) Dg²⁴⁸, sli² has cardioblast phenotype (Qian et al., 2005) Dg²⁴⁸/Dg[+], sli² has cardioblast phenotype (Qian et al., 2005) dlg1[+]/dlg1¹, sli² has cardioblast phenotype (Qian et al., 2005) dlg1¹, sli² has cardioblast phenotype (Qian et al., 2005) Mtl^Δ, sli² has longitudinal connective phenotype (Fan et al., 2003, Fan et al., 2003) Pak^{Scer\UAS.T:Hsap\MYC}, Scer\GAL4^elav.PLu, sli² has longitudinal connective phenotype (Fan et al., 2003, Fan et al., 2003) Pak^{Scer\UAS.T:Myr-Src64B}, Scer\GAL4^elav.PLu, sli² has longitudinal connective phenotype (Fan et al., 2003, Fan et al., 2003) Rac1^J11, sli² has longitudinal connective phenotype (Fan et al., 2003, Fan et al., 2003) Rac1^N17.Scer\UAS, Scer\GAL4^elav.PLu, sli² has longitudinal connective phenotype (Fan et al., 2003, Fan et al., 2003) Rac1^N17.Scer\UAS, Scer\GAL4^ftz.ng, sli² has longitudinal connective phenotype (Fan et al., 2003, Fan et al., 2003) Rac2^Δ, sli² has longitudinal connective phenotype (Fan et al., 2003, Fan et al., 2003) Rho1^N19.Scer\UAS, Scer\GAL4^elav.PLu, sli² has longitudinal connective phenotype (Fan et al., 2003, Fan et al., 2003) Rho1^N19.Scer\UAS, Scer\GAL4^ftz.ng, sli² has longitudinal connective phenotype (Fan et al., 2003, Fan et al., 2003) robo[+]/robo¹, sli² has medial longitudinal fascicle \| ectopic phenotype (Garbe et al., 2007) robo[+]/robo⁴, sli² has lateral multidendritic neuron ldaA phenotype (Parsons et al., 2003) robo[+]/robo⁴, sli² has lch5 neuron phenotype (Parsons et al., 2003) robo[+]/robo⁴, sli² has lesA neuron phenotype (Parsons et al., 2003) robo¹, sli² has longitudinal connective \| embryonic stage 16 phenotype (Keleman et al., 2005) robo¹, sli² has midline crossing tract \| embryonic stage 16 phenotype (Keleman et al., 2005) robo¹, sli² has presumptive embryonic/larval central nervous system phenotype (Kidd et al., 1999, Kidd et al., 1999) robo⁴, sli² has lateral multidendritic neuron ldaA phenotype (Parsons et al., 2003) robo⁴, sli² has lch5 neuron phenotype (Parsons et al., 2003) robo⁴, sli² has lesA neuron phenotype (Parsons et al., 2003) robo⁴, sli² has presumptive embryonic/larval central nervous system phenotype (Kidd et al., 1999, Kidd et al., 1999) Scer\GAL4^elav.PLu, sli², unc-5^{Scer\UAS.T:Ivir\HA1,T:SS-wg} has anterior commissure phenotype (Keleman and Dickson, 2001, Keleman and Dickson, 2001, Keleman and Dickson, 2001) Scer\GAL4^elav.PLu, sli², unc-5^{Scer\UAS.T:Ivir\HA1,T:SS-wg} has posterior commissure phenotype (Keleman and Dickson, 2001, Keleman and Dickson, 2001, Keleman and Dickson, 2001) Sdc[+]/Sdc^unspecified, sli² has A1-7 lateral transverse muscle \| supernumerary phenotype (Steigemann et al., 2004) Sdc^unspecified, sli² has A1-7 lateral transverse muscle \| supernumerary phenotype (Steigemann et al., 2004) shg[+]/shg², sli² has cardioblast phenotype (Qian et al., 2005) shg², sli² has cardioblast phenotype (Qian et al., 2005)
Additional Comments
Genetic Interactions
Statement Reference sli[2]/+ Sac1[1]/+ double heterozygotes show a high frequency of ectopic midline crossings in the central nervous system. (Lee et al., 2011) sli[2]/+ suppresses the dorsal branch fusion phenotype seen when Sdc[dsRNA.Scer\UAS.cSa] is expressed under the control of Scer\GAL4[btl.PS]. One copy of sli[2] partially suppresses the dorsal branch fusion phenotype seen in the tracheal system of Sdc[2639] homozygous third instar larvae. One copy each of sli[2] and Sdc[2639] does not produce any dorsal branch fusion defects. (Schulz et al., 2011) kuz[H143], sli[2] transheterozygous stage 16 embryos display a stronger ectopic ap neuron crossing phenotype than either mutant alone. kuz[2583]/+ enhances the ectopic ap neuron crossing phenotype seen in sli[2] heterozygous stage 16 embryos. kuz[112]/+ enhances the ectopic ap neuron crossing phenotype seen in sli[2] heterozygous stage 16 embryos. Expression of kuz[DN.Scer\UAS] in ipsilateral ap neurons under the control of Scer\GAL4[ap-md544] in a sli[2]/+ mutant background produces more severe ap axon midline crossing defects in stage 16 embryos than in either mutant alone. (Coleman et al., 2010) Blocking vg function through expression of sd[Δ88-159.Scer\UAS] in ventral longitudinal muscle cells (under the control of Scer\GAL4[Mef2.PR]) that abnormally migrate along the midline owing to a sli[2] mutant background, leads to fewer and smaller muscle-muscle adhesions. Increasing vg function through expression of vg[2.Scer\UAS] in ventral longitudinal muscle cells (under the control of Scer\GAL4[Mef2.PR]) that abnormally migrate along the midline owing to a sli[2] mutant background, leads to more and larger muscle-muscle adhesion sites. Increasing vg function through expression of vg[2.Scer\UAS] in somatic muscle cells (under the control of Scer\GAL4[Mef2.PR]) of sli[2] mutants greatly enhances the adhesion level between the midline-crossing ventral longitudinal muscles. Expression of Egfr[DN.Scer\UAS] in somatic muscle cells (under the control of Scer\GAL4[Mef2.PR]) of sli[2] mutants decreases the size and/or number of adhesion sites along the midline. (Deng et al., 2010) The longitudinal tract midline crossing phenotype seen in comm^unspecified mutants is significantly enhanced by sli²/+, both in terms of the numbers of segments and the number of embryos affected. (Bhat et al., 2007) sli², robo¹/+ embryos show midline axon guidance defects, with on average two to three medial longitudinal fascicle ectopically crossing the midline per embryo. β-Spec^em6/Y; sli², robo¹/+ show an enhancement of the midline axon guidance defects seen in β-Spec^em6/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-Spec^G0074/Y; sli², robo¹/+ and β-Spec^G0198/Y; sli², robo¹/+ triple mutant embryos. Expression of β-Spec^{Scer\UAS.T:Hsap\MYC}, under the control of Scer\GAL4^elav.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-Spec^em6/Y; sli²/+ and β-Spec^G0198/Y; sli²/+ embryos, although the timing at which the defects appear is not altered. Expression of β-Spec^{Scer\UAS.T:Hsap\MYC} under the control of Scer\GAL4^ap-md544 is unable to rescue the β-Spec^em6/Y; sli²/+ phenotype back to the sli²/+ severity. (Garbe et al., 2007) Expression of fra[ΔC.Scer\UAS.T:Ivir\HA] driven by Scer\GAL4[elav.PLu] in a fra[unspecified] sli[2] double mutant background results in a phenotype similar to the phenotype observed for overexpression of fra[ΔC.Scer\UAS.T:Ivir\HA] in a fra[unspecified] single mutant background, where many axons fail to cross the midline. (Garbe et al., 2007) 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. (Lee et al., 2007) Reduction of sli in a sli[2] heterozygous background leads to a fused commissures phenotype in elav[5] mutant embryos. (Simionato et al., 2007) 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, LanA^9-32, wb^SF11, vkg¹⁷⁷, vkg^P10038 and rhea¹. The following alleles produce a mild heart phenotype when doubly heterozygous with lea², lea^S4-18, Nrt^M54 and Ras85D⁰⁵⁷⁰³. Ilk^ZCL3111/+; 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: mew^M6/+; sli²/+ embryos, Tig^x/+, sli²/+ embryos and dock⁰⁴⁷²³/+, sli²/+ embryos. Dorsal closure is delayed in sli²/+, scb⁰¹²⁸⁸/+ embryos but is complete at hatching. (MacMullin and Jacobs, 2006) In egh⁷/Y; sli²/+ mutants, the R-cell axonal projection pattern is defective like in egh⁷ single mutants. egh⁷/+; sli²/+ mutants appear wild type. (Fan et al., 2005) In robo[1],sli[2] /+,+ stage 16 embryos, FasII axons cross the midline in three to five segments per embryo. Expression of Nedd4[Scer\UAS.T:Hsap\MYC] under the control of either Scer\GAL4[elav.PLu] or Scer\GAL4[1407] does not enhance the midline crossing phenotype seen in transheterozygous sli[2] robo[1] stage 16 embryos. Expression of Nedd4[EY00500] under the control of either Scer\GAL4[elav.PLu] or Scer\GAL4[1407] does not enhance the midline crossing phenotype seen in transheterozygous sli[2] robo[1] stage 16 embryos. Df(3R)ED4688 does not enhance the midline crossing phenotype seen in transheterozygous sli[2] robo[1] stage 16 embryos. Expression of ena[Scer\UAS.cCa] under the control of Scer\GAL4[elav.PLu] suppresses the midline crossing phenotype seen in transheterozygous sli[2] robo[1] stage 16 embryos. (Keleman et al., 2005) In sli²; fra³/fra⁴ double mutants, the penetrance of the salivary gland guidance defects is reduced by 40% compared to sli² single mutants. (Kolesnikov and Beckendorf, 2005) 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. (Qian et al., 2005) The transformation of abdominal lch5 chordotonal organs to a morphology resembling thoracic dch3 chordotonal organs that is seen in larvae expressing lea^EP2582 under the control of Scer\GAL4^elav-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 25^oC. (Kraut and Zinn, 2004) sli² chb⁴ double heterozygous embryos have axons ectopically crossing the midline. sli² chb^P4 double heterozygous embryos have axons ectopically crossing the midline. (Lee et al., 2004) 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. (Orgogozo et al., 2004) sli² Sdc^unspecified 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%). Sdc^unspecified homozygous embryos that are also heterozygous for sli² show an enhanced axonal guidance defect with multiple midline crossings of the fascicles. (Steigemann et al., 2004) The combination of heterozygous sli² and pan-neural overexpression of Rho1^N19.Scer\UAS (expressed under the control of Scer\GAL4^elav.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 Rho1^N19.Scer\UAS is driven by Scer\GAL4^ftz.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 Rac1^N17.Scer\UAS (expressed under the control of Scer\GAL4^elav.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 Rac1^N17.Scer\UAS is driven by Scer\GAL4^ftz.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 Cdc42^N17.Scer\UAS (expressed under the control of Scer\GAL4^elav.PLu) does not cause longitudinal axon ectopic midline crossing defects. The combination of heterozygous sli² and pan-neural overexpression of Pak^{Scer\UAS.T:Myr1} under the control of Scer\GAL4^elav.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 Pak^{Scer\UAS.T:Hsap\MYC} under the control of Scer\GAL4^elav.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 Pak^{Scer\UAS.T:Myr1} partially suppresses longitudinal axon ectopic midline crossing defects seen in sli²/+, Rac1^N17.Scer\UAS ; Scer\GAL4^elav.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 Rac1^J11 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 Rac2^Δ 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 Mtl^Δ 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. (Fan et al., 2003) 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. (Parsons et al., 2003) The ch neurons in sli²/+ robo3¹/+ embryos frequently show abnormal projections. (Zlatic et al., 2003) 98% of lola^ORE120 sli²/lola^ORE120 embryos show Fas2-expressing axons crossing the midline. There are an average of 4.8 crossovers per affected embryo. (Crowner et al., 2002) sli² robo^unspecified 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 mew^M6/+ sli²/+ double heterozygous mutants the frequency of midline guidance errors is increased over the level observed in mew^M6 homozygous mutants. Less than 10% of segments revealed midline guidance errors in mew^M6/+ sli²/+ embryos. (Stevens and Jacobs, 2002) 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 capt^B99, capt^k01217, capt¹⁰ or Abl². (Wills et al., 2002) Percentage of segments with midline crossovers in robo¹/sli² transheterozygotes is 45%. (Battye et al., 2001) When sli²/sli² is in combination with unc-5^{Scer\UAS.T:Ivir\HA1,T:wg}, Scer\GAL4^elav.PLu the interaction is difficult to interpret - collapse of longitudinal fibers onto the midline is hindered, but midline cells are still displaced. (Keleman and Dickson, 2001) The lateral transverse muscles make normal attachments in 98% of segments in embryos expressing robo^Scer\UAS.cKa under the control of Scer\GAL4^how-24B that are also mutant for sli². (Kramer et al., 2001) 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 lea^X123 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 lea^X123 triple mutant embryos. (Kramer et al., 2001) The penetrance of the midline crossover phenotype of Fas2-positive axons in heterozygous embryos is enhanced by one copy of Sos^e49. (Fritz and VanBerkum, 2000) The addition of lea^EP2582 (driven by Scer\GAL4^elav.PLu) to homozygous sli² embryos has no effect on the embryonic ventral nerve cord phenotype seen in these embryos. (Rajagopalan et al., 2000) The Ptp10D¹; Ptp69D¹/Ptp69D^8ex25 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. (Sun et al., 2000) Embryos heterozygous for both robo¹ and sli² show deviation of longitudinal fascicles towards the midline in 74% of segments. (Battye et al., 1999) 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. (Kidd et al., 1999) Dominantly suppresses the wing blister phenotype of if³ flies. (Wessendorf et al., 1992)
Xenogenetic Interactions
Statement Reference Fas2-positive axon bundles cross the midline in 100% of sli²/+ embryos which are also expressing Ggal\MLCK^ct.Scer\UAS under the control of Scer\GAL4^ftz.ng. (Kim et al., 2002) The penetrance of the Fas2-positive axon crossover phenotype is increased in sli² embryos that also carry Khc::Ggal\MLCK^KA.ftz compared to either single mutant alone. (Fritz and VanBerkum, 2000)
Complementation & Rescue Data
Rescued by	sli²/sli^k04807b is rescued by Scer\GAL4^bi-md653/sli^Scer\UAS.cKa (Tayler et al., 2004) sli² is rescued by sli^Scer\UAS.cKa/Scer\GAL4^sim.P3.7 (Orgogozo et al., 2004)
Partially rescued by	sli² is partially rescued by Scer\GAL4^B2-3-30/sli^Scer\UAS.cBa (MacMullin and Jacobs, 2006) sli² is partially rescued by Scer\GAL4^B2-3-30/sli^{ΔL1-L4.Scer\UAS} (MacMullin and Jacobs, 2006) sli² is partially rescued by Scer\GAL4^Mef2.PR/sli^Scer\UAS.cKa (Santiago-Martinez et al., 2006) sli² is partially rescued by Scer\GAL4^sim.P3.7/sli^Scer\UAS.cBa (Battye et al., 1999) sli² is partially rescued by Scer\GAL4^sli.PS/sli^Scer\UAS.cBa (Battye et al., 2001) sli² is partially rescued by sli^Scer\UAS.cKa/Scer\GAL4^sim.P3.7 (Kramer et al., 2001, Kramer et al., 2001) sli² is partially rescued by sli^Scer\UAS.cKa/Scer\GAL4^sli.PS (Kidd et al., 1999) sli² is partially rescued by sli^{ΔE2-E6.Scer\UAS}/Scer\GAL4^sli.PS (Battye et al., 2001) sli² is partially rescued by sli^{ΔG-E7.Scer\UAS}/Scer\GAL4^sli.PS (Battye et al., 2001)
Not rescued by	sli² is not rescued by sli^{ΔL1-L4.Scer\UAS}/Scer\GAL4^sli.PS (Battye et al., 2001)
Comments	Expression of either sli^Scer\UAS.cBa or sli^{ΔL1-L4.Scer\UAS} under the control of Scer\GAL4^B2-3-30 leads to a significant recovey in heart cell morphology. (MacMullin and Jacobs, 2006) Expression of sli^Scer\UAS.cKa under the control of Scer\GAL4^Mef2.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. (Santiago-Martinez et al., 2006) The midline is rescued in sli² embryos expressing sli^Scer\UAS.cKa under the control of Scer\GAL4^sim.P3.7. (Kramer et al., 2001)
Stocks ( 2 )
Bloomington	3266 cn¹ sli² bw¹ sp¹/CyO
Kyoto	106948 w¹¹¹⁸; cn¹ sli² bw¹ sp¹ / CyO; TM6B, Tb¹
Notes on Origin
Discoverer

Comments
	Protein null. (Battye et al., 2001)
External Crossreferences & Linkouts
Other Crossreferences

Linkouts

Synonyms & Secondary IDs ( 7 )
Reported As
Symbol Synonym	sli² (MacMullin and Jacobs, 2006, Christensen and Cook, 2007.5.8, Vanderploeg et al., 2012, Christensen et al., 2007.10.29, Lee et al., 2007, Lee et al., 2007, Harris and Beckendorf, 2007, Sano et al., 2005, Bhat et al., 2007, Wayburn and Volk, 2009, Weyers et al., 2011) sli^IG7 (Tearle and Nusslein-Volhard, 1987, ) sli^IG107 (Kolodziej et al., 1995, Sonnenfeld and Jacobs, 1995, Sonnenfeld and Jacob, 1994, Wessendorf et al., 1992, Jacobs, 1993, Klambt et al., 1991, Nambu et al., 1990, ) slit (Fan et al., 2003) slit² (Fan et al., 2003, Kraut and Zinn, 2004, Johnson et al., 2004, Steigemann et al., 2004, Parsons et al., 2003, Zlatic et al., 2003, Wills et al., 2002, Kim et al., 2002, Keleman and Dickson, 2001, Battye et al., 2001, Kramer et al., 2001, Kidd et al., 1999, Garbe et al., 2007, Simionato et al., 2007, Dimitrova et al., 2008, Coleman et al., 2010, Keleman et al., 2005, Schulz et al., 2011, Lee et al., 2011) slit^IG107 (Crowner et al., 2002, Zhou et al., 1997, Therianos et al., 1995) unnamed (Kramer et al., 2001)
Name Synonym	slit² (Santiago-Martinez et al., 2006, Garbe et al., 2007, Deng et al., 2010)
Secondary FlyBase IDs

References ( 62 )

Generate a list of	All references relating to this allele ( 62 )

List References by type	Research paper ( 57 ) Supplementary material ( 2 ) Personal communication to FlyBase ( 2 ) Stock list ( 1 )
Recent research papers ( 4 )
	Vanderploeg et al., 2012, BMC Dev. Biol. 12: 8 Integrins are required for cardioblast polarisation in Drosophila. [FBrf0217831] Lee et al., 2011, Mol. Cells 32(5): 477--482 The phosphoinositide phosphatase Sac1 is required for midline axon guidance. [FBrf0216733] Schulz et al., 2011, EMBO Rep. 12(10): 1039--1046 Drosophila syndecan regulates tracheal cell migration by stabilizing Robo levels. [FBrf0216287] Weyers et al., 2011, Dev. Biol. 353(2): 217--228 A genetic screen for mutations affecting gonad formation in Drosophila reveals a role for the slit/robo pathway. [FBrf0213539] Show all research papers ...

Allele Dmel\sli2

Allele Dmel\sli²