Sema-1a, Sema 1a, D-SemaI, SemaI, semaphorin
axon guidance transmembrane protein - motor axons requiring Sema-1a for choice-point defasciculation - Sema-1a reverse signaling promotes midline crossing in response to secreted semaphorins - prevents Drosophila olfactory projection neuron dendrites from mis-targeting into select antennal lobe regions
Please see the JBrowse view of Dmel\Sema1a for information on other features
To submit a correction to a gene model please use the Contact FlyBase form
AlphaFold produces a per-residue confidence score (pLDDT) between 0 and 100. Some regions with low pLDDT may be unstructured in isolation.
Tissue-specific extension of 3' UTRs observed during later stages (FBrf0218523, FBrf0219848); all variants may not be annotated
Gene model reviewed during 5.44
Alternative translation stop created by use of multiphasic reading frames within coding region.
Stop-codon suppression (UGA) postulated; FBrf0216884.
Annotated transcripts do not represent all supported alternative splices within 5' UTR.
Gene model reviewed during 5.45
Gene model reviewed during 5.56
Click to get a list of regulatory features (enhancers, TFBS, etc.) and gene disruptions (point mutations, indels, etc.) within or overlapping Dmel\Sema1a using the Feature Mapper tool.
The testis specificity index was calculated from modENCODE tissue expression data by Vedelek et al., 2018 to indicate the degree of testis enrichment compared to other tissues. Scores range from -2.52 (underrepresented) to 5.2 (very high testis bias).
Comment: maternally deposited
Sema1a expression is first detected at embryonic stage 10 and reaches a peak at stage 16. It is expressed in most CNS neurons. It is weakly expressed in the PNS, mainly in lateral sensory clusters.
Sema1a is widely expressed in the thoracic neuromere but expression decreases towards the midline where it is at its lowest.
Sema1a is first detected in sensory neuropil at embryonic stage 13 and persists until the end of embryogenesis. The highest levels are in the lateral and intermediate portions of layers 1 and 3, with lower levels in layer 2 and none in layer 4 (layers 1-4 defining four regions in the dorsal/ventral axis with 1 being the dorsal-most layer).
Sema1a protein is expressed in the cell bodies and axons of the photoreceptors in the lamina, medulla and optic stalk. It also labels axons of other cells in the medulla.
In the late third instar larva, Sema1a protein is diffusely distributed in brain, preferentially in the optic lobes. Sema1a protein is also expressed in the thoracic segments of the ventral nerve cord, and at the midline of the thoracic and abdominal segments. At prepupal stages, Sema1a protein is localized to the central brain, optic lobes, subesophageal neuromere, connectives, and the thoracic neuromeres. At mid-pupal stages when the giant fiber--tergotrochanteral muscle motor neuron synapses are forming, the Sema1a expression pattern becomes more refined. At these stages, Sema1a protein is localized to several layers of the medulla, the alpha and alpha' lobes of the mushroom body, and the outer neuropil of the neuromeres. Expression fades in later pharate adult stages.
Comment: low expression throughout adult brain
JBrowse - Visual display of RNA-Seq signals
View Dmel\Sema1a in JBrowse2-33
2-28.6
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 JBrowse 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.
Sema-1a-mediated motor axon defasciculation is promoted by pbl and inhibited by RhoGAPp190. The opposing pbl and RhoGAPp190 functions mediate Sema-1a reverse signaling through the regulation of Rho1 activity.
otk appears to ne an important component for repulsive signalling in response to Semaphorin ligands in axon guidance.
Sema-1a mediates axonal guidance defasciculation events by acting as an axonally localised repellent.
Sema-1a is required for the correct guidance of motor axons and for the formation of central nervous system pathways.
Sema-1a encodes a transmembrane protein whose distribution suggests a function in axon guidance.
Identified on basis of similarity to grasshopper semaphorin.
Source for merge of: Sema-1a BcDNA:RE36155
Source for merge of Sema-1a BcDNA:RE36155 was a shared cDNA ( date:030728 ).
Source for identity of: Sema1a Sema-1a