l(2)05248, CT37068, CT21700, dSlit
extracellular - egf like - ligand of Roundabout - regulates axon guidance - Slit-dependent endocytic trafficking of the Robo receptor is required for Son of Sevenless recruitment and midline axon repulsion - Dscam1 forms a complex with Robo1 and the N-terminal fragment of Slit to promote the growth of longitudinal axons
Gene model reviewed during 5.44
Stop-codon suppression (UGA) postulated; FBrf0216885.
Low-frequency RNA-Seq exon junction(s) not annotated.
Gene model reviewed during 5.50
Interacts with robo.
Click to get a list of regulatory features (enhancers, TFBS, etc.) and gene disruptions (point mutations, indels, etc.) within or overlapping Dmel\sli using the Feature Mapper tool.
sli is first detected during gastrulation. At germ band extension, midline mesectodermal cells express sli. During germ band retraction, sli is detected in the 6 midline glial cells derived from the midline neurepithelium. During dorsal closure, sli expression is detected in cardioblasts, walls of the gut, and near the muscle attachment.
sli is first detected at the cellular blastoderm stage, where it is confined to the presumptive ectoderm. After gastrulation, sli expression is detected in the lateral ectoderm in a segmentally repeated pattern, and in the midline neurepithelium. Lower levels of expression are detected in the developing gut. Expression in the contracted germ band stage is in a metameric pattern along the CNS midline, abutting the neuropil. At stage 17, expression is detected in the neuropil between longitudinal and commissural nerve bundles.
Immuno-EM staining of stage 16 embryos identified sli protein on the lumenal surface of the hindgut boundary cells, which correlated in size and shape to microvilli structures.
sli is expressed in posterior escort cells, FSCs, and immediate daughter cells, but not in older germarial follicle cells
sli is detected in class 1 and class IV dendritic arborizing neurons in larvae. It is also detected in muscles and in some other dendritic arborizing neurons.
Low levels of sli protein are detected in the commissures and longitudinal connectives starting at embryonic stage 12. sli protein from the midline is initially taken up by the commissural axon tracts when they cross the midline and is transported along the commissural tracts into the longitudinal connectives.
sli protein distribution in the extracellular space was examed with detergenet-free immunocytochemistry. At embryonic stage 13 there is a gradient of sli protein that steeply descends from its midline source. Once the neuropil begins to develop, there is an accumulation of sli at around 10 microns from the midline, where the longitudinal fascicles begin to develop. By hour 14, this accumulation reaches 43% of midline levels. Subsequently, sli levels rise continuously at both the midline and neuropils. The aCC dendrites develop at the site of the sli enrichment and immediately after, but not before nor long after, local sli concentrations begins to rise there.
sli protein is observed in a sheet of cells in the midline of the developing subesophageal ganglion.
sli protein is enriched in the extracellular matrix of S2 cells.
sli protein was detected in the body wall epidermis in a broad pattern in the dorsal and lateral aspect in embryonic stages 13-15. sli protein could no longer be detected at stage 16 in the epidermis. Expression of sli in the central nervous system midline was detectable from stages 13-16.
The sli transcript and protein expression patterns coincide. sli protein is first detected during gastrulation. At germ band extension, midline mesectodermal cells express sli protein. During germ band retraction, sli protein is detected in the 6 midline glial cells derived from the midline neurepithelium. During dorsal closure, sli protein expression is detected in cardioblasts, walls of the gut, and near the muscle attachment sites in the ectoderm. Using immunoelectron microscopy, sli protein is detected along the axons of commissural and longitudinal axon tracts, but not in the cell bodies supplying these axons, suggesting that sli protein is secreted from the midline glial cells and becomes associated with the axons which traverse the midline.
sli protein is first detected in the midline neurepithelium after germ band extension. During germ band shortening, expression becomes restricted to median ectodermal cells (MECs). After germ band contraction is complete, sli protein is detected in MECs, the axon commissures they surround, and longitudinal connectives. In supraesophageal segments, strong axon labelling is detected, and this labelling seems to be on the cell surface.
GBrowse - Visual display of RNA-Seq signalsView Dmel\sli in GBrowse 2
Please Note FlyBase no longer curates genomic clone accessions so this list may not be complete
Please Note This section lists cDNAs and ESTs that fall within the genomic extent of the gene model, which may include cDNAs and ESTs of genes within introns, or of overlapping genes. Please see GBrowse for alignment of the cDNAs and ESTs to the gene model.
For each fully sequenced cDNA the DGRC maintains various forms of the cDNA (e.g tagged or untagged) in several different host vectors for subsequent cloning and expression in Drosophila and Drosophila cell lines.
New annotation (CG33464) in release 3.2 of the genome annotation.
sli is required to prevent migration of thoracic chordotonal organs during development so that they remain in a dorsal position in the thorax.
sli is required to prevent ventral multidendritic vmd1a sensory cells from crossing the midline during development of the nervous system.
dsRNA made from templates generated with primers directed against this gene tested in RNAi screen for effects on Kc167 and S2R+ cell morphology.
sli functions as a chemorepellent at the midline and as a chemoattractant at muscle attachment sites for migrating mesoderm cells.
sli signalling promotes the terminal symmetric division of neural precursor cells in the CNS.
Mutants show medial collapse of lateral axon tracts and ectopic midline crossing of ventral muscles. Ectopic expression of sli inhibits formation of axon tracts and misdirects axon tracts towards the midline.
Axon and muscle cell growth cone repulsion from the midline of the CNS requires sli.
Ten EMS induced alleles were identified in a screen for mutations affecting commissure formation in the CNS of the embryo.
sli appears to act as a short-range repellent controlling axon crossing of the midline and as a long-range chemorepellent controlling mesoderm migration away from the midline.
Dorsal median cells fail to persist in sli mutants: CNS midline cells are required for dorsal median cell development.
Mutations in 12 complementation groups differentially affect lateral chordotonal axon growth, fasciculation or ventral orientation. Mutations in robo, spen, sli and los cause lch axon defasciculation. Mutations in sli and los also cause some lch axon bundles to grow dorsally along a trajectory 180o from normal.
The differentiation of individual mesectoderm cells (MECs) lineages is traced. Mutations in sli affect the position but not the differentiation or survival of the MECs, establishing that misposition of the MECs is sufficient to cause complete collapse of the longitudinal axon tracts.
Sequence analysis of sim Tl and sli revealed a conserved sequence ACGTG that resembles the mammalian xenobiotic response element. This motif forms the core of an element required for CNS midline transcription.
Cys poor regions of the proteins encoded by sli and ft are homologous with the laminin A-type modules of the crb protein.The laminin A-type modules of these proteins may participate in the interactions that control morphogenesis.
Mutant embryos exhibit defective development of cells derived from the mesectoderm and severe fusion of the embryonic CNS.