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General Information
Symbol
Dmel\Fas2e76
Species
D. melanogaster
Name
FlyBase ID
FBal0029778
Feature type
allele
Associated gene
Associated Insertion(s)
Carried in Construct
Also Known As
FasIIe76
Nature of the Allele
Mutations Mapped to the Genome
 
Type
Location
Additional Notes
References
Associated Sequence Data
DNA sequence
Protein sequence
 
 
Cytology
Nature of the lesion
Statement
Reference
Imprecise excision of the P-element from Ecol\lacZFas2-A31.
Expression Data
Reporter Expression
Additional Information
Statement
Reference
 
Marker for
Reflects expression of
Reporter construct used in assay
Human Disease Associations
Disease Ontology (DO) Annotations
Models Based on Experimental Evidence ( 0 )
Disease
Evidence
References
Modifiers Based on Experimental Evidence ( 0 )
Disease
Interaction
References
Comments on Models/Modifiers Based on Experimental Evidence ( 0 )
 
Phenotypic Data
Phenotypic Class
Phenotype Manifest In
Detailed Description
Statement
Reference
Fas2e76/Fas2e76, Fas2e76/Fas2EB112 or Fas2e76/Df(1)BSC869 larval NMJs all have fewer synaptic boutons than controls. Fas2e76/+ NMJs have no change in bouton number compared to controls.
The wings of Fas2e76 mutants raised at 18[o]C are abnormally elongated. Fas2EB112/Fas2e76 adults display a rough-eye phenotype. Ommatidial photoreceptor and cone cell numbers are disrupted, and in some cases mini-clusters of ommatidia are observed.
When Fas2 is simultaneously decreased in both pre- and post-synaptic cells in Fas2e76 heterozygotes, the result is a small but significant increase in bouton number. This change in bouton number is not attributable to changes in muscle size, which is indistinguishable from wild-type controls. Satellite bouton number in Fas2e76 heterozygotes decreases to 33% the wild-type value. These bouton buds are similar to those observed in wild-type, including the distribution of synaptic vesicles, active zones, and post-synaptic specialisations. Fas2e76/+ heterozygotes exhibit EJPs with significantly larger amplitudes than wild-type controls.
The motor neuron that innervates DLMa has a higher number of contact points with the muscle in Fas2e76 mutants; there is an average of 5.8 contact points in Fas2e76 mutants vs. 4-6 in wild type. This phenotype also occurs in Fas2e76/Fas2EB112 transheterozygotes: these mutants have an average of 6 contact points per DLMa. The DLMa is 11% longer in Fas2e76/Fas2EB112 mutants than wild type. Investigation of adult innervation pattern in Fas2e76/Fas2EB112 mutants shows that outgrowth of secondary branches is not affected, but that branch elaboration, which occurs at 18-24 hours APF, is affected. During this stage, the average length of Fas2e76/Fas2EB112 secondary branches is increased, as is the area occupied by the higher order arbors of the secondary branches. Additionally, a higher level of secondary branches are stabilized, as shown by staining for futsch, in Fas2e76/Fas2EB112 mutants at 24 hours APF than wild type.
Fas2e76 mutants exhibit normal axon patterns. There are sporadic single BM axon defects, but no OP axon alterations are found. Fas2e76/Fas2EB112 mutants exhibit normal axon patterns. There are sporadic single BM axon defects, but no OP axon alterations are found.
Synaptic bouton number is significantly reduced at the NMJs of third instar larval Fas2e76 mutants.
The increase in frequency seen in the synaptic drive to aCC/RP2 during the first 28hr of larval life is not affected in the hypomorphic Fas2e76.
Heterozygous Fas2e76/+ flies, in which Fas2 levels are ~50% of wild-type, exhibit a striking increase in bouton number. Homozygous Fas2e76 flies do not exhibit an additional increase in bouton number.
In 14% of the mushroom bodies of mutant animals, an abnormal lobe morphology is seen.
The number of boutons at the neuromuscular junction is reduced by 34% in Fas2e76 larvae compared to wild type.
The morphology of the larval visual system (LVS) is disrupted in most homozygous embryos. Disruption of Bolwig's organ (BO) development can be seen as early as stage 13, when unclustered photoreceptor cells can be seen located near the normal BOs. Later defects include BOs that are smaller than normal, failure of BOs to migrate properly and the presence of nodules along the nerve in some embryos.
The RP3 and 6/7b neurons which innervate longitudinal muscles 6 and 7 have reduced terminals and fewer but larger varicosities in Fas2e76 mutant larvae compared to wild-type.
The morphology of the subsynaptic reticulum at type I boutons appears normal in hemizygous flies. There is an increase in the number of active zones within type I boutons.
Fas2e76/Fas2e93 transheterozygotes exhibit a 50% increase in number of MN boutons at muscle 6. Mild heat induced expression of CrebB-17Aa.hs during larval stages significantly increases the quantal content of the synapse without altering quantal size (as shown by measuring excitatory postsynaptic potential, EPSP). Homozygotes exhibit a 30%-40% reduction in number of boutons, mild heat induced expression of CrebB-17Aa.hs during larval stages does not change the quantal content of the synapse.
In homozygous embryos the SNb fails to diverge from the ISN partially (partial bypass) in 6% segments.
Growth of the synapse reduces when Fas2 expression level is low causing a drop in number of boutons. In Fas2e76/Fas2e93 transheterozygotes growth of the synapse increases as Fas2 expression level is low causing a rise in number of boutons.
Mutant exhibits a reduced number of nerve terminal varicosities at third instar larval neuromuscular junctions. Assaying synaptic transmission demonstrates there is no major alteration in synaptic strength at the whole muscle cell level in these mutants. Ultrastructural characteristics of individual synapses are adjusted to counteract the reduction in the number of nerve terminal varicosities, thereby maintaining the physiological properties of transmission.
Homozygous heads often appear wild type, one or both postvertical bristle can be missing, at 17oC both bristles are missing. Transheterozygotes with Fas2EB112 exhibit missing postvertical, ocellar, vertical and orbital bristles. At 17oC the phenotype is more penetrant with missing ocelli.
Striking defasciculation of the FN3 pathway axons.
Normal grooming behaviour.
Homozygotes show reduced viability. Transheterozygotes for Fas2EB112 and Fas2e76 are sterile. Increased branching of wing sensory axons in discs during metamorphosis. Ectopic sensory neurons are displayed in the wing.
At embryonic stage 12/1 and early stage 13, the MP1, dMP2 and vMP2 growth cones are stalled in Fas2e76 mutants, as is seen in Fas2EB112 and Fas2eB78 mutants. However by late stage 13 and early stage 14, these growth cones often extend towards each other and fasiculate, although in a delayed and variable way, in Fas2e76 mutants. In Fas2e76 mutants, different segments within the same embryo can display different lengths of MP1 extension and differences in axon trajectories. Nevertheless, the MP1 pathway ultimately forms in most segments in Fas2e76 mutants.
External Data
Interactions
Show genetic interaction network for Enhancers & Suppressors
Phenotypic Class
Enhanced by
Statement
Reference
Suppressed by
Statement
Reference
Fas2e76 has neuroanatomy defective | dominant phenotype, suppressible | partially by rl[+]/rl10a
Enhancer of
Suppressor of
Statement
Reference
Fas2e76 is a suppressor of neuroanatomy defective phenotype of sei2
Other
Phenotype Manifest In
Enhanced by
Statement
Reference
Fas2EB112/Fas2e76 has eye phenotype, enhanceable by aosΔ7
Fas2e76 has NMJ bouton | larval stage phenotype, enhanceable by Amph26
Suppressed by
Statement
Reference
Fas2e76 has NMJ bouton phenotype, suppressible by Appld
Fas2e76 has bouton | supernumerary phenotype, suppressible | partially by rl[+]/rl10a
Fas2e76 has bouton phenotype, suppressible by sifES11
NOT suppressed by
Statement
Reference
Fas2e76 has bouton | supernumerary phenotype, non-suppressible by rl[+]/rlSem
Enhancer of
Statement
Reference
Fas2[+]/Fas2e76 is an enhancer of ocellar nerve phenotype of Nrgl3
Fas2e76 is an enhancer of NMJ bouton | larval stage phenotype of Amph26
NOT Enhancer of
Statement
Reference
Fas2[+]/Fas2e76 is a non-enhancer of mechanosensory neuron phenotype of Nrgl3
Suppressor of
Statement
Reference
Fas2e76 is a suppressor of NMJ bouton | supernumerary phenotype of sei2
Fas2e76 is a suppressor of neuromuscular junction phenotype of sei2
Fas2e76 is a suppressor of NMJ bouton | supernumerary phenotype of slo1
Fas2[+]/Fas2e76, Scer\GAL4C164 is a suppressor of NMJ bouton phenotype of Applsd.UAS, Scer\GAL4C164
Fas2e76 is a suppressor of bouton phenotype of sifES11
NOT Suppressor of
Statement
Reference
Fas2e76 is a non-suppressor of neuromuscular junction phenotype of slo1
Other
Additional Comments
Genetic Interactions
Statement
Reference
Fas2e76/Y or Fas2e76/Fas2G0293 third instar larvae with GluRIICdsRNA.Scer\UAS.cBa driven by Scer\GAL4C57 do not show impairment of homeostatic compensation at the neuromuscular junction (significant reduction in mEPSP and significant increase in quantal content compared to controls, just as is seen in larvae with expression of GluRIICdsRNA.Scer\UAS.cBa driven by Scer\GAL4C57). GluRIIASP16/GluRIIASP16;Cskc04256/Cskj1D8 Fas2e76 third instar larvae also show a small significant increase in bouton number per muscle area (segment A2, synapse 6/7).
Animals heterozygous for both Fas2e76 and beag1 have a 42% decrease in NMJ synaptic bouton number compared with wild type, whereas the single heterozygotes show no change in bouton number. Combining beag1/Df(3R)Exel6151 with heterozygous or homozygous Fas2e76 does not further decrease bouton number compared with beag1/+ alone.
Fas2e76 ; Gfrldel/Gfrldel, Fas2e76 ; Gfrldel/Df(3R)Exel6185 and Fas2e76 ; Gfrldel/Df(3R)BSC518 double mutant males are completely infertile.
Fas2e76/sei2 double mutants exhibit significantly reduced satellite levels compared to sei2 single mutants, more pronouncedly for type M than type B satellites. The frequency of mature boutons and complexity of terminal branches is also affected in these mutants. Bouton number is reduced in these mutants. The frequency of satellite formation in Fas2e76; slo1 double mutants is comparable to slo1 single mutants. Overall bouton number is slightly reduced in these double mutants. However, a similar reduction is seen in Fas2e76 mutants.
The rough-eye phenotype observed in Fas2EB112/Fas2e76 flies is enhanced by the presence of argosΔ7/+.
The increase in bouton number in Fas2e76/+ heterozygotes is completely suppressed in Appld homozygous mutants. Indeed, the number of synaptic boutons is lower than in wild-type. The increased EJP amplitude in Fas2e76/+ heterozygotes is completely suppressed in the absence of Appl in Appld, Fas2e76/+ mutants. The EJP is indistinguishable from Appld/+ mutants. A Fas2e76 background suppresses the increase in bouton number observed when Applsd.Scer\UAS is overexpressed pre-synaptically (under the control of Scer\GAL4C164).
A heterozygous Fas2e76 background acts as a dominant enhancer of the Nrgl3 defects in OP axons at the restrictive temperature. The axonal guidance defects of BM axons in Nrgl3 are not affected.
Bouton numbers are further reduced at the NMJs of third instar larvae in Fas2e76;Amph26 double mutants.
The increase in bouton number observed in Fas2e76/+ heterozygotes is partially suppressed by rl10a/+ mutants. Double mutants of Fas2e76 rlSem do not exhibit a bouton number significantly different from that found in the Fas2e76 mutant alone.
Fas2e76 does not rescue the sideD609 phenotype; defasciculation by the ISNb axons at muscle 28 is 8.5% in sideD609 single mutants and 7.6% in sideD609 Fas2e76 double mutants.
The number of boutons at the neuromuscular junction is restored to wild type in Fas2e76 sifES11 double mutant larvae. The number of boutons at the neuromuscular junction is extremely reduced in Fas2e76 embryos expressing sifScer\UAS.cSa under the control of Scer\GAL4elav.PLu.
The defects in development of the larval visual system seen in both beat-Iatric-1 and Fas2e76 single mutants are partly suppressed in Fas2e76 ; beat-Iatric-1 double mutants; the LVS develops normally in the majority of double mutant embryos and the defects seen are relatively minor.
Partially dominantly suppresses the central nervous system phenotype of Df(4)C3 embryos. Also suppresses the ISNb motor axon phenotypes, but not the SNa axon phenotypes of Df(4)C3 embryos.
Fas2e93; beat-Ia2 flies have a moderate beat-Ia phenotype, 41% segments have a divergence defect. The divergence defect of beat-Ia3 is also significantly suppressed by Fas2e76.
Xenogenetic Interactions
Statement
Reference
Complementation and Rescue Data
Comments
Scer\GAL4Rapgap1-OK6-mediated expression of Fas2C.Scer\UAS does not rescue the reduced bouton number of Fas2e76/Df(1)BSC869 animals. Scer\GAL4Rapgap1-OK6-mediated expression of Fas2Scer\UAS.cLb fully rescues the reduced bouton number of Fas2e76/Df(1)BSC869 animals. Scer\GAL4Rapgap1-OK6-mediated expression of Fas2Scer\UAS.cLa fully rescues the reduced bouton number of Fas2e76/Df(1)BSC869 animals.
Expression of Fas2Scer\UAS.cLa can rescue the DLMa innervation phenotype of Fas2e76 mutants, depending on the driver used. Under the control of Scer\GAL4elav-C155, Fas2Scer\UAS.cLa reduces the average number of motor neuron contact points along the DLMa in Fas2e76 mutants from 5.8 to 5.1, while this number is reduced to 4.6 when Fas2Scer\UAS.cLa is driven by Scer\GAL4Mhc.PW.
Scer\GAL4E62-2 mediated expression of Fas2Scer\UAS.cLa rescues bouton reduction where Scer\GAL4 is expressed (muscle 3).
The defasciculation phenotype can be rescued by Scer\GAL4 driven expression of Fas2 : the FN3 axons refasciculate.
Images (0)
Mutant
Wild-type
Stocks (0)
Notes on Origin
Discoverer
Comments
Comments
Mutation resulting from the imprecise excision of a nearby P element.
External Crossreferences and Linkouts ( 0 )
Synonyms and Secondary IDs (6)
References (36)