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General Information
Symbol
Dmel\Fas2EB112
Species
D. melanogaster
Name
FlyBase ID
FBal0029776
Feature type
allele
Associated gene
Associated Insertion(s)
Carried in Construct
Also Known As
fasIIEB112
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. 1.7kb deletion of Fas2 genomic sequences, including 5' untranslated sequences. The deletion is entirely within the Fas2 gene and is likely to include the start of transcription. Genomic sequences more than 1kb from the 5' end of the Fas2 gene are unaffected.
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
fascicle & mushroom body | somatic clone
synapse & aCC neuron
synapse & RP2 neuron
thorax & macrochaeta | somatic clone
thorax & microchaeta | somatic clone
U neuron & growth cone
Detailed Description
Statement
Reference
Fas2EB112/Fas2EB112 mushroom body clones have normal axon pruning.
Fas2e76/Fas2EB112 larval NMJs have fewer synaptic boutons than controls. Fas2EB112/+ NMJs have no change in bouton number compared to controls.
Anterior follicle cells in homozygous follicle cell clones undergo normal cell shape changes during oogenesis.
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. Fas2EB112 mutant eye clones show cone cell defects, defects in photoreceptor cell number, and mini-ommatidia are observed. Fas2EB112 mutant clones in eye disc display abnormal elav-positive cell clusters between ommatidia which resemble R7-like photoreceptor cells. Some of the cells associated with the ectopic clusters are genotypically wild-type. No R8 photoreceptor cells are associated with the ectopic cell clusters. Loss of function clones of Fas2EB112 in the adult notum display one or more ectopic dorsocentral bristles. other macro- and microchaetae are largely unaffected. Extra sensory organ precursor cells are observed in Fas2EB112 mutant clones.
Fas2EB112 homozygous adults generally have normal mushroom body lobes, but occasionally have a misdirected alpha lobe. Fas2EB112/Fas2e86 transheterozygotes do not have mushroom body lobe defects in the adult.
There are no obvious abnormalities in the timing and dynamics of the myopodia-filopodia interactions to form the synaptic contact site in Fas2EB112/Y embryos. In these mutants, T-shaped presynaptic terminals of normal size form in the prospective synaptic site along the proximal edge of target muscle 12.
Fas2EB112 mutants exhibit amorphous and expanded tracheal tubes, where the luminal chitin does not organise correctly, in comparison to wild-type
The motor neuron that innervates DLMa has a higher number of contact points with the muscle in Fas2e76/Fas2EB112 mutants (6) than in wild type (5). 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/Fas2EB112 mutants exhibit normal axon patterns. There are sporadic single BM axon defects, but no OP axon alterations are found.
In a Fas2EB112 mutant background, U motorneuron growth cones exhibit a wide shape that is reminiscent of aCC/RP2 pioneer growth cones.
In stage 14 Fas2EB112 mutants, the lumenal chitin in the developing dorsal trunk of the tracheal system fails to form a filamentous cable running along the tube length, as in wild-type, but instead is amorphous and fills the lumen.
In Fas2EB112 homozygotes, the border follicle cells lose their polarity. Delamination of these cells is delayed, but their migration is accelerated.
Mutant embryos develop long and convoluted tracheal dorsal trunks and the apical cell surface of the dorsal trunk cells appears elongated and expanded. Tubular dilations are seen in the transverse connectives and the lumen of several tracheal branches is discontinuous.
During the first 28hr of wild-type larval life, the frequency of suprathreshold synaptic drive to aCC/RP2 increases considerably. In the absence of Fas2, such as in Fas2EB112, the frequency of synaptic drive to aCC/RP2 still increases during this period, although this increase is significantly less than when Fas2 is present. In Fas2EB112 mutants the number of presynaptic terminals that contact aCC remains unchanged. The ultrastructure of the presynaptic terminals at this stage is qualitatively indistinguishable from those that develop in wild-type.
The initial growth of the pioneer mushroom body (MB) axons is not disturbed in mutants. After converging at the protocerebral neuropil, the MB axons exhibit a normal medial turn and from the primordial medial lobe. When homozygous mutant clones are made in the MB, the axon projections exhibit no gross abnormalities. However dispersed axonal fascicles are seen in 23% of cases, in which axon bundles are randomly scattered throughout the axonal layers of the peduncle and lobes.
Fas2EB112/+ embryos have normal axon guidance.
Larvae successfully hatch and begin crawling around but within hours begin to behave sluggish and uncoordinated, they ultimately stop moving and die. Synapses form and mature but in the absence of Fas2 they do not grow and then retract, the number of boutons drops to a few or zero.
Transheterozygotes with Fas2e76 exhibit missing postvertical, ocellar, vertical and orbital bristles. At 17oC the phenotype is more penetrant with missing ocelli. Gynandromorph mosaics demonstrate hemizygous male regions fail to differentiate the postvertical, ocellar and vertical bristles and still have some orbital bristles. Ocelli are missing and the compound eye has a rough phenotype. Some macro- and microchaetes in the thorax are missing.
EM analysis of the extent of fasciculation and membrane apposition between various pairs of axons reveals normal neurite outgrowth, extension and guidance in embryos. Some aspects of selective fasciculation and axon-glia interactions appear highly abnormal, the vMP2, MP1 and FN3 pathways defasciculate. Scer\GAL4 driven expression of Fas2 can refasciculate the FN3 axons.
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.
The MP1 pathway does not form in Fas2EB112 mutant embryos: at embryonic stage 12/1 the dMP2 and MP1 growth cones do not turn posteriorly (which happens in the wild-type) but rather project laterally for a short distance. Also, the vMP2 growth cone often turns anteriorly (as in the wild-type) but already shows variability in the precise orientation of its tip. The MP1, dMP2 and vMP2 growth cones stay stalled in the same position through to stage 14 in mutant embryos, in contrast to the wild-type.
External Data
Interactions
Show genetic interaction network for Enhancers & Suppressors
Phenotypic Class
Phenotype Manifest In
Enhanced by
Statement
Reference
Fas2EB112/Fas2e76 has eye phenotype, enhanceable by aosΔ7
Suppressed by
Statement
Reference
Enhancer of
Statement
Reference
Fas2EB112/Fas2[+] is an enhancer of eye phenotype of rhohs.sev
NOT Enhancer of
Statement
Reference
Suppressor of
Statement
Reference
Fas2EB112/Fas2[+] is a suppressor of eye phenotype of Scer\GAL4sev.EP, styUAS.cHa
Fas2EB112 is a suppressor of synapse & RP2 neuron phenotype of Ctet\tetXTNT-LC.UAS, Scer\GAL4eve.RRK
Fas2EB112 is a suppressor of synapse & aCC neuron phenotype of Ctet\tetXTNT-LC.UAS, Scer\GAL4eve.RRK
Fas2EB112/Fas2[+] is a suppressor of RP3 neuron & synapse phenotype of Sema1ak13702
Fas2EB112/Fas2[+] is a suppressor of intersegmental nerve phenotype of Sema1ak13702
NOT Suppressor of
Statement
Reference
Other
Additional Comments
Genetic Interactions
Statement
Reference
Fas2EB112/Fas2EB112 significantly suppresses the axon pruning defect caused by bskLL02244/bskLL02244 (mushroom body clones).
Large follicle cell clones doubly homozygous for Taoeta and Fas2EB112 show cell lethality, while small follicle cell clones doubly homozygous for Taoeta and Fas2EB112 can be recovered in stage 8/9 egg chambers. Anterior follicle cells in these small clones stretch normally.
The glial cell migration defects of rapie28 embryos are significantly suppressed by Fas2EB112 (54.7% of hemisegments show normal migration, 27.9% of hemisegments show partial migration). However, the increase in glial cell number and the axonal defects seen in rapie28 embryos is not suppressed by Fas2EB112.
rhohs.sev rough eye phenotype is enhanced in the presence of Fas2EB112/+ at 18[o]C. Expression of EgfrScer\UAS.cBa under the control of Scer\GAL4GMR.PF results in a rough-eye phenotype, which is enhanced by the presence of Fas2EB112/+. The rough-eye phenotype observed in Fas2EB112/Fas2e76 flies is enhanced by the presence of argosΔ7/+. The rough-eye phenotype observed in flies expressing styScer\UAS.cHa under the control of Scer\GAL4sev.EP is suppressed in the presence of Fas2EB112/+.
Intersegmental nerves are co-arrested upon expression of RdlScer\UAS.cSa in the aCC/RP2 neurons (under the control of Scer\GAL4eve.RN2) in a Fas2EB112 mutant background in 36% of cases, compared with 70% in a wild-type background.
In the absence of Fas2, in Fas2EB112 mutants, the effect of Ctet\TeTxLCTNT.Scer\UAS expression in aCC/RP2 neurons (under the control of Scer\GAL4eve.RRK) on the frequency of synaptic inputs is significantly diminished compared to Ctet\TeTxLCTNT.Scer\UAS expression in wild-type.
Fas2EB112/+, Kr1/+ double heterozygotes (that also carry KrmCD) exhibit an axon guidance phenotype. The SNb enters the ventral muscle field normally in most cases but the nerve stops at the second choice point by forming a growth cone-like structure. No individual RP axons are observed.
The intersegmental nerve b (ISNb) phenotypes seen in homozygous Sema-1ak13702 embryos are suppressed by one copy of Fas2EB112. Synaptic arborisations on ventral lateral muscles (VLMs) 12 and 6-7 appear normal. The Sema-1ak13702 segmental nerve a (SNa) defasciculation defects are not suppressed by Fas2EB112 alone. However, rescue of the Sema-1ak13702 SNa stall phenotype is seen in Fas2EB112/+ ; Sema-1ak13702 ; ConFvex238 triple mutant embryos; the SNa dorsal branches bifurcate at lateral muscles (LMs) 22-23 and extend dorsally. Sema-1ak13702 CNS defects are suppressed by one copy of Fas2EB112 (they are seen in only 10% of hemisegments, compared to 31% in Sema-1ak13702 single mutants).
Xenogenetic Interactions
Statement
Reference
Complementation and Rescue Data
Comments
Scer\GAL4elav.PLu or Scer\GAL4Mhc.PW mediated expression of Fas2Scer\UAS.cLa rescues larval lethality. Scer\GAL4A51 mediated expression of Fas2Scer\UAS.cLa causes mosaic rescued larvae, rescue of boutons in the segments Scer\GAL4 is expressed (muscles 6 and 7) and elimination of boutons in segments where it is not expressed.
Images (0)
Mutant
Wild-type
Stocks (1)
Notes on Origin
Discoverer
External Crossreferences and Linkouts ( 0 )
Synonyms and Secondary IDs (14)
References (36)