FasII, Fasciclin II, Fas II, 1D4, FasciclinII
Gene model reviewed during 5.52
Annotated transcripts do not represent all possible combinations of alternative exons and/or alternative promoters.
Gene model reviewed during 5.48
Gene model reviewed during 5.55
Gene model reviewed during 6.01
3.070, 2.818 (longest cDNA)
None of the polypeptides share 100% sequence identity.
873, 811 (aa); 97, 90 (kD predicted)
Click to get a list of regulatory features (enhancers, TFBS, etc.) and gene disruptions (point mutations, indels, etc.) within or overlapping Dmel\Fas2 using the Feature Mapper tool.
Fas2-XP is excluded from the calyx of the larval mushroom body, but not from the lobes.
Fas2 is enriched in fascicles in the neuropile and motor axons outside the CNS, but very low or absent in somatodendritic areas and nerve roots.
Fas2 protein is strongly upregulated just posterior to the morphogenetic furrow in third instar eye discs. After this initial strong expression in the preclusters, Fas2 expression is low in distinct ommatidial cluster patterns in the cell membranes of most photoreceptors. Eventually, elevated levels of Fas2 protein are seen just in one of the photoreceptor cells, namely R7.
. At late L3, Fas2-expressing cells appear at the boundary of tarsal region 5 and the pretarsus.
Fas2 is used a marker for immature larval photorecetor cells of Bolwig organ.
In stage 12 embryos, Fas2 protein is detected in the primordium of the pars lateralis. In the larva, it labels the axons of the dorsomedial and anteriolateral neurosecretory cells which form the pars intercerebralis and pars lateralis, respectively.
Fas2 is present in the periactive zone of the presynapse, but does not precisely colocalize with Dap-160, endoA, or dynamin.
In the adult prothorax and neck, Fas2 immunoreactivity is observed in the type II boutons of motorneurons innervating ventral cervical muscle 27 and prothoracic sternal anterior rotator muscle 31, but is undetectable in terminals located along the cuticle of the coxal midline. Fas2 is not detected at type I boutons of adult prothoracic neuromuscular junctions, unlike the pattern observed in larval neuromuscular junctions. Fas2 immunoreactivity is also observed in the trunk and branches of the cervical nerve, and in the glial cells surrounding the cervical nerve.
Fas2 protein is expressed in the three longitudinal fascicles of the embryonic longitudinal connectives, and in peripheral motor neurons.
In the developing germarium, Fas2 protein is expressed in all follicle cells during early oogenesis. At stage 7, Fas2 protein becomes apically localized in follicle cells, then is lost in migrating border follicle cells, while being localized to the leading edge of polar follicle cells.
Fas2 is found in the more mature mature, non-core neurons of the pedunculus of the 3rd instar larvae.
Expression in procephalic neuroblasts stage 9-11: tritocerebrum - d1, d2, d6, v1-3; deuterocerebrum - d9, d11, v2, v8
Fas2 protein is strongly expressed in the mushroom body alpha and beta lobes, and weakly in the mushroom body gamma-lobe and spur.
At stage 12, two neurons in each hemisphere express Fas2 protein, aCC and pCC. At this stage, the pCC growth cone which pioneers the MP1 pathway expresses Fas2 protein. By stage 13, it is expressed in other cells along the MP1 pathway. By stage 14, the MP1 pathway is continuous from segment to segment and Fas2 protein is expressed along its length as well as in some axons of the intersegmental nerve root including aCC. By stage 16, Fas2 protein is expressed in other longitudinal axon pathways. Outside of the CNS, it is expressed in the periphery in several motoneuron growth cones in each hemisegment including the aCC growth cone. In the PNS, it is expressed in some sensory neurons in most segments. It is expressed in patches in the ectoderm that will give rise to the spiracles, in Malpighian tubules, in the part of the hindgut bordering the Malpighian tubules and in ectodermal patches in the head.
GBrowse - Visual display of RNA-Seq signalsView Dmel\Fas2 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.
Source for identity of: Fas2 CG3665
Source for merge of: Fas2 l(1)G0081 l(1)G0048 l(1)G0032 l(1)G0336 l(1)G0293
FlyBase curator comment: Correspondence with author Guntur confirmed that 'FAS 11' = 'Fas2' (CG3665).
Duplicate transcripts identified and eliminated during the migration of annotations from the release 5 genome assembly to the release 6 assembly.
Fas2 has a role in stabilizing branches during dorsal medial muscle innervation.
Fas2 is required in the neurosecretory cells innervating the corpus allatum for normal genitalia rotation in males.
Fas2 is required for the normal development of the lobes and the underlying structure of the mushroom body.
Fas2 has a role in the molecular operations encoding short-term odour memories and conferring alcohol sensitivity.
The C-terminal sequences of Fas2 and Sh are both necessary and sufficient for targeting to the subsynaptic muscle membrane at the larval neuromuscular junction, and this localization depends on the product of dlg1.
CrebB-17A acts in parallel with Fas2 to cause an increase in synaptic strength. cAMP initiates these parallel changes to achieve long-term synaptic enhancement. Expression of the CrebB-17A repressor in the dnc mutant blocks functional but not structural plasticity. Expression of the CrebB-17A activator increases synaptic strength, but only in Fas2 mutants that increase bouton number, due to increased presynaptic transmitter release. Expression of CrebB-17A in a Fas2 mutant background genetically reconstitutes cAMP-dependent plasticity. Thus, cAMP initiates parallel changes in CrebB-17A and Fas2 to achieve long-term synaptic enhancement.
After synapse formation, the homophilic cell adhesion molecule Fas2 is localised both pre- and postsynaptically where it controls synapse stabilization. In null mutants synapse formation is normal but boutons retract during larval development. Synapse elimination and resulting lethality are rescued by transgenes that drive Fas2 expression both pre- and postsynaptically, expression on either side alone is not sufficient. Fas2 can also control synaptic growth.
Downstream regulation of synaptic Fas2 expression is both necessary and sufficient for the long-term synaptic sprouting induced by increase in neuronal activity or increase in cAMP levels. Fas2 down-regulation on its own is not sufficient to alter synaptic strength, down regulation is therefore a step in the pathway controlling a purely structural component in the events of synaptic plasticity. Events downstream of cAMP must in part control the concomitant changes in synaptic function during long-term synaptic plasticity.
The expression pattern of proneural genes of the AS-C and neurogenic genes of the E(spl)-C are examined in the procephlon and a map of the cells is constructed.
Fas2 is required for induction of proneural gene expression in certain locations of the eye-antennal imaginal disc.
Fas2 is required for proper morphogenesis of the neuromuscular junction. The size of the synaptic zone can be changed by altering the levels of Fas2. Results suggest Fas2 may play an important role in mediating structural changes during the activity-dependent events of synaptic plasticity.
Changes in the pattern and level of Fas2 expression can alter growth cone guidance. Four classes of abnormal phenotypes can be caused by ectopic expression of Fas2 : "bypass" phenotypes, where axons fail to defasciculate at the choice point where they would normally enter their muscle target region; "detour" phenotypes, where bypass growth cones enter their muscle target region at a different location, "stall" phenotypes, where axons that enter their muscle target region fail to defasciculate from one another to probe their muscle targets; and "misroute" phenotypes, in which growth cones are diverted onto abnormal pathways by contact with Fas2-positive cells.
Loss of function Fas2 mutations lead to the complete or partial defasciculation of the vMP2, MP1 and FN3 pathways. This mutant phenotype can be rescued by overexpression of Fas2. This overexpression can alter fasciculation by abnormally fusing pathways together. The results define an in vivo function for Fas2 as a neuronal recognition molecule that controls one mechanism of growth cone guidance - selective axon fasciculation - and genetically separates this function from other aspects of outgrowth and directional guidance.
The phenotypes of Fas1, Fas2, Fas3 and nac mutants were analysed in the developing wing: the axon tracts in the CNS for the most part remain unaltered, and none of the phenotypes are 100% penetrant, indicating a fine-tuning role for these molecules in both the PNS and CNS.
Antibody to Fas2 used in a screen for mutations affecting neuromuscular connectivity.