FB2026_03 , released September 17, 2026
Allele: Dmel\Fas2UAS.PEST-
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General Information
Symbol
Dmel\Fas2UAS.PEST-
Species
D. melanogaster
Name
FlyBase ID
FBal0044814
Feature type
allele
Associated gene
Associated Insertion(s)
Carried in Construct
Also Known As
UAS-FasII, UAS-FasII-A-PEST-
Key Links
Nature of the Allele
Progenitor genotype
Carried in construct
Cytology
Description

UASt sequences regulate expression of the coding sequence of the PEST- transmembrane isoform of Fas2.

Allele components
Component
Use(s)
Encoded product / tool
Mutations Mapped to the Genome
Curation Data
Type
Location
Additional Notes
References
Variant Molecular Consequences
Associated Sequence Data
DNA sequence
Protein sequence
 
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 ( 1 )
Disease
Interaction
References
Comments on Models/Modifiers Based on Experimental Evidence ( 0 )
 
Disease-implicated variant(s)
 
Phenotypic Data
Phenotypic Class
Phenotype Manifest In

synapse & abdominal 2 ventral longitudinal muscle 1, with Scer\GAL4elav-C155

synapse & abdominal 3 ventral longitudinal muscle 1, with Scer\GAL4elav-C155

synapse & abdominal 4 ventral longitudinal muscle 1, with Scer\GAL4elav-C155

synapse & abdominal 5 ventral longitudinal muscle 1, with Scer\GAL4elav-C155

synapse & abdominal 6 ventral longitudinal muscle 1, with Scer\GAL4elav-C155

synapse & abdominal 7 ventral longitudinal muscle 1, with Scer\GAL4elav-C155

Detailed Description
Statement
Reference

Overexpression of Fas2Scer\UAS.cLa by Scer\GAL4Tab2-201Y results in significant axon (but not dendrite) pruning defects.

Scer\GAL4Rapgap1-OK6-mediated expression of Fas2Scer\UAS.cLa induces a significant increase in NMJ synaptic bouton number.

Scer\GAL4elav.PU Fas2Scer\UAS.cLa embryos display a high degree of ISNb hyperfasciculation.

Expression of Fas2UAS.cLa under the control of Scer\GAL4c739 results in defects in mushroom body lobes in some adults; this can include lobes extending in the wrong direction, thicker lobes, thinner lobes, missing lobes and ectopic masses of axons at the tip of the peduncle, none of these phenotypes occur in control animals. Expression of Fas2UAS.cLa under the control of Scer\GAL4c739 does not affect mushroom body lobe structure in the larva, but can cause defects in the peduncle; during early metamorphosis, some alpha' lobes collapse, this is correlated with misdirection of the alpha lobe and does not occur in controls. Expression of Fas2UAS.cLa under the control of Scer\GAL4Tab2-201Y does not lead to mushroom body lobe defects in the larva or the adult. Expression of Fas2UAS.cLa under the control of Scer\GAL4NP2082 does not lead to mushroom body lobe defects in the larva or the adult. Expression of Fas2UAS.cLa under the control of Scer\GAL4ey-OK107 leads to a lack of extension of any mushroom body lobes (including gamma, alpha', beta', alpha and beta) in any direction from the peduncle and the formation of a mass of axons at the tip of the peduncle in the adult brain. In the larva, expression of Fas2UAS.cLa under the control of Scer\GAL4ey-OK107 sometimes results in a thinner dorsal lobe or a shift of the core of the peduncle closer to the border of the peduncle.

When Fas2Scer\UAS.cLa is driven by Scer\GAL4elav-C155, severe morphological abnormalities are seen in the third instar mushroom bodies. Both the dorsal and medial lobes are markedly affected. The core is also disrupted. When Fas2Scer\UAS.cLa is driven by Scer\GAL4OK107, developmental defects are seen in the majority of mushroom bodies. When Fas2Scer\UAS.cLa is driven by Scer\GAL4Tab2-201Y, no mushroom body defects are seen. When Fas2Scer\UAS.cLa is driven by Scer\GAL4238Y, only mild defects are seen in mushroom bodies. Medial lobes terminate in single blob but internally harbour three branches.

Embryos expressing Fas2Scer\UAS.cLa under the control of Scer\GAL4elav-C155 show modest hyperfasciculation defects in the intersegmental nerve b (ISNb).

Scer\GAL4how-24B-mediated expression promotes muscle-muscle adhesion in vivo at a high level. Extensive muscle-muscle adhesion between subsets of ventral muscles causes defects in innervation, SNb axons reach the target region normally but the terminal abors on the internal muscle surface are greatly reduced. No abnormality in SNb axon trajectory is seen, they enter the ventral muscle field at the correct choice point and extend toward the target region normally.

Extra bristles in the vicinity of the postvertical bristles and other regions of the adult fly.

In a P{GawB}elavC155 background the SNb axons are dramatically affected, showing bypass, stall and detour phenotypes. SNa axons are also affected, showing predominantly stall mutant phenotypes. The ISN also shows a misrouting phenotype. Axons extend from below muscle 12 to synapse on the outside, dorsal surface of the fiber: the "reach-back" phenotype In a P{GawB}C38 background causes extensive ISN growth cone exploration of and adhesive contact to the tracheal cells which is never observed in wild type. The ISN can extend past the main tracheal trunk and the contacts are withdrawn in late stage 16.

Scer\GAL4ftz.ng expression causes a novel gain of function FN3/MP1 fused pathway phenotype at stage 16 (fused phenotype is not continuous but rather occurs for short stretches) and fused vMP2 and MP1 pathways at stage 14.

External Data
Interactions
Show genetic interaction network for Enhancers & Suppressors
Phenotypic Class
Enhanced by
Suppressed by
NOT Suppressor of
Phenotype Manifest In
Additional Comments
Genetic Interactions
Statement
Reference

Co-expression of Fas2Scer\UAS.cLa, Fas2Scer\UAS.cLb or Fas2C.Scer\UAS in third instar larvae with GluRIICdsRNA.Scer\UAS.cBa simultaneously driven by Scer\GAL4C57 and Scer\GAL4elav-C155 does not impair 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 simultaneously driven by Scer\GAL4C57 and Scer\GAL4elav-C155).

Co-expression of bskDN.Scer\UAS.cUa enhances axon-pruning defects in flies with Fas2Scer\UAS.cLa driven by Scer\GAL4Tab2-201Y.

Scer\GAL4Rapgap1-OK6-mediated expression of Fas2Scer\UAS.cLa does not rescue synaptic bouton number or average synaptic bouton area of beag1/Df(3R)Exel6151 animals.

The intersegmental nerve b (ISNb) phenotypes seen in homozygous Sema-1ak13702 embryos are enhanced by Fas2Scer\UAS.cLa expressed under the control of Scer\GAL4elav-C155. The ISNb may fail to defasciculate from the intersegmental nerve (ISN) which results in a fusion bypass with the ISN. ISNb is also seen to stall ventrally on ventral lateral muscles (VLMs) 6-7. The number of hemisegments showing aberrant or absent RP3 innervation of VLMs 6 and 7 is increased. A failure of RP1, RP4 and RP5 to defasciculate around VLMs 13 and 6, a "stall" phenotype, is also increased. Sema-1ak13702 SNa phenotypes are dramatically enhanced by Fas2Scer\UAS.cLa expressed under the control of Scer\GAL4elav-C155. Failure of all SNa lateral branches to defasciculate from the SNa pathway, resulting in the lack of SNa lateral branches, is seen. An increase in the stall phenotype of the dorsal SNa branch is also seen.

Xenogenetic Interactions
Statement
Reference
Complementation and Rescue Data
Comments

Scer\GAL4Rapgap1-OK6-mediated expression of Fas2Scer\UAS.cLa fully rescues the reduced bouton number of Fas2e76/Df(1)BSC869 animals.

Scer\GAL4 induced expression rescues the lethality of Fas2EB112.

Images (0)
Mutant
Wild-type
Stocks (0)
Notes on Origin
Discoverer
External Crossreferences and Linkouts ( 0 )
Synonyms and Secondary IDs (4)
Reported As
Symbol Synonym
Fas2Scer\UAS.cLa
Fas2UAS.PEST-
Fas2UAS.cLa
Name Synonyms
Saccharomyces cerevisiae UAS construct a of Lin
Secondary FlyBase IDs
    References (20)