Sema-2a, SemaII, semaphorin, sema-II, D-SemaII
Gene model reviewed during 5.50
Annotated transcripts do not represent all supported alternative splices within 5' UTR.
Low-frequency RNA-Seq exon junction(s) not annotated.
Gene model reviewed during 5.55
4.0 (northern blot)
Interacts with PlexB.
Click to get a list of regulatory features (enhancers, TFBS, etc.) and gene disruptions (point mutations, indels, etc.) within or overlapping Dmel\Sema2a using the Feature Mapper tool.
Sema2a expression is first detected at embryonic stage 10 in weak epidermal stripes. It is also found in the CNS starting in stage 15 in a restricted set of neurons. Beginning in stage 14, Sema2a is expressed in a single ventral thoracic muscle fiber in the metathoracic segment. Expression occurs also in embryonic gonads and anterior sense organs.
Sema2a is widely expressed in the thoracic neuromere and expression increases towards the midline where it peaks.
Sema2a protein is expressed in the medial and ventromedial antennal lobe. This pattern is similar to the one of Sema2b protein, except that the gradient of Sema2a protein is steeper than the one of Sema2b. The level of expression of Sema2a is opposite to the one of Sema-1a : if the expression level of Sema2a is high, the one of Sema-1a is low, and vice-versa.
Sema2a is first detected in sensory neuropil at embryonic stage 14, persists until stage 16, and is gone by stage 17. The highest levels are in layer 2 at the center of the neuropile (layers 1-4 defining four regions in the dorsal/ventral axis with 1 being the dorsal-most layer). The protein forms gradients of expression that extend dorsally and ventrally from layer 2. No expression is observed in layer 4.
GBrowse - Visual display of RNA-Seq signalsView Dmel\Sema2a 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.
Sema-2a and Sema-2b are both ligands of the plexB receptor, but they have different guidance functions during neurogenesis. Sema-2b functions at short-range as a guidance cue to promote axonal attraction, mediating axon-axon recognition and fasciculation, whereas Sema-2a acts over a broader range as a repulsive cue, to prevent aberrant innervation.
Mutants isolated in a screen of the second chromosome identifying genes affecting disc morphology.
Sema-2a prevents promiscuous and ectopic synapse formation. Relative balance of Sema-2a and Fas2 controls synaptogenesis. The relative balance of Sema-2a and the Netrins controls the choice of a specific target and the avoidance of a potential target. NetB and Sema-2a can both be repulsive for certain motor axons.
Sema-2a can function as a inhibitory signal during target recognition, it inhibits two identified motoneuron growth cones RP3 and DC1 from forming normal synaptic terminal aborizations on their target muscles. RP1 and RP4 are unresponsive to contact with Sema-2a.
Genetic analysis reveals that semaII is an essential gene required for both proper adult behaviour and survival.