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General Information
Symbol
Dmel\Fas2UAS.cLa
Species
D. melanogaster
Name
Saccharomyces cerevisiae UAS construct a of Lin
FlyBase ID
FBal0044814
Feature type
allele
Associated gene
Associated Insertion(s)
Carried in Construct
Also Known As
UAS-FasII, UAS-Fas2, UAS-Fas II, UAS-fasciclinII
Allele class
Nature of the Allele
Allele class
Mutations Mapped to the Genome
 
Type
Location
Additional Notes
References
Associated Sequence Data
DNA sequence
Protein sequence
 
 
Progenitor genotype
Carried in construct
Cytology
Nature of the lesion
Statement
Reference
Expression of the Fas2 PEST cDNA is governed by UAS regulatory sequences.
Allele components
Product class / Tool use(s)
Encoded product / tool
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
axon & eye photoreceptor cell, with Scer\GAL4GMR.PF
eye photoreceptor cell & lamina, with Scer\GAL4GMR.PF
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.
Expression of Fas2Scer\UAS.cLa in a Df(2R)eve mutant background, under the control of Scer\GAL4eve.RN2 leads to both aCC and RP2 motor neurons displaying an almost exclusively single exit from the CNS.
Scer\GAL4Rapgap1-OK6-mediated expression of Fas2Scer\UAS.cLa induces a significant increase in NMJ synaptic bouton number.
Expression of Fas2Scer\UAS.cLa under the control of Scer\GAL4let-7-C does not alter mushroom body α/β lobe morphology. Expression of Fas2Scer\UAS.cLa under the control of Scer\GAL4c305a results in α'/β' mushroom body lobe neurons projecting into the α/β lobe.
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.
In late third instar Fas2Scer\UAS.cLa; Scer\GAL4GMR.PF larvae, the axons of eye photoreceptor cells are hyperfasciculated.
The number of secondary branches on the motor neuron that innervates DLMa is reduced when Fas2Scer\UAS.cLa is expressed under the control of the neuronal Scer\GAL4elav-C155 driver. As a result, the pool of secondary branches that can form higher order branches is reduced and the number of contact points between the neuron and the muscle is significantly reduced (from 5 to 4.3). When Fas2Scer\UAS.cLa is expressed in muscle, under the control of Scer\GAL4Mhc.PW, there is a reduction in the amount of secondary branches on the motor neuron that innervates DLMa. However, secondary branches are longer and occupy a greater area on the muscle surface than wild-type branches. The lower numbers of secondary branches results in a lower number of contact points between the neuron and the muscle (from 5 to 4.4) and a reduction in overall muscle length.
In Fas2Scer\UAS.cLa; Scer\GAL4BA3 flies the border follicle cells have much reduced polarity. Delamination of these cells is delayed (they initiate migration behind the trailing edge of the epithelium) but their migration rate is normal.
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
Enhancer of
NOT Suppressor of
Other
Phenotype Manifest In
Enhanced by
Statement
Reference
Suppressed by
Enhancer of
Statement
Reference
Fas2UAS.cLa is an enhancer of axon & eye photoreceptor cell phenotype of Scer\GAL4GMR.PF/Scer\GAL4GMR.PF, Sema1aUAS.cYa
Fas2UAS.cLa is an enhancer of axon & lamina phenotype of Scer\GAL4GMR.PF/Scer\GAL4GMR.PF, Sema1aUAS.cYa
Fas2UAS.cLa is an enhancer of eye photoreceptor cell & lamina phenotype of Scer\GAL4GMR.PF/Scer\GAL4GMR.PF, Sema1aUAS.cYa
Fas2UAS.cLa is an enhancer of axon & medulla phenotype of Scer\GAL4GMR.PF/Scer\GAL4GMR.PF, Sema1aUAS.cYa
Fas2UAS.cLa is an enhancer of eye photoreceptor cell & medulla phenotype of Scer\GAL4GMR.PF/Scer\GAL4GMR.PF, Sema1aUAS.cYa
Fas2UAS.cLa is an enhancer of nerve terminal & lamina plexus phenotype of Scer\GAL4GMR.PF/Scer\GAL4GMR.PF, Sema1aUAS.cYa
Scer\GAL4elav-C155/Fas2UAS.cLa is an enhancer of RP3 neuron & synapse phenotype of Sema1ak13702
NOT Suppressor of
Other
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.
Expression of Fas2Scer\UAS.cLa in an eveΔRP2A mutant background results in the exit of a single motoneuron of the pair in each hemisegment. These mutants exhibit an increase in dorsal projections in 25% of hemisegments. Co-expression of unc-5Scer\UAS.T:Ivir\HA1,T:SS-wg and Fas2Scer\UAS.cLa in a Df(2R)eve mutant background, under the control of Scer\GAL4eve.RN2 leads to a more robust CNS exit for motor neurons, with many hemisegments displaying exit of both motor neurons. There are two types of exit: unfasciculated, both axons from the same hemisegment chose a different nerve root, or fasciculated, where axons join and exit through the intersegmental nerve root. Co-expression of unc-5Scer\UAS.T:Ivir\HA1,T:SS-wg, beat-IaScer\UAS.cFa and Fas2Scer\UAS.cLa in a Df(2R)eve mutant background, under the control of Scer\GAL4eve.RN2 leads to a more robust CNS exit for motor neurons, with many hemisegments displaying exit of both motor neurons. The number of hemisegments with one neuronal exit is reduced, compared to controls and single and double mutants. Co-expression of beat-IaScer\UAS.cFa and Fas2Scer\UAS.cLa in a Df(2R)eve mutant background, under the control of Scer\GAL4eve.RN2 leads to a more robust CNS exit for motor neurons, with many hemisegments displaying exit of both motor neurons. There are two types of exit: unfasciculated, both axons from the same hemisegment chose a different nerve root, or fasciculated, where axons join and exit through the intersegmental nerve root.
Expression of Fas2Scer\UAS.cLa fails to suppress the synaptic retraction phenotype seen in the NMJs of third instar larvae when NrgGD82 is expressed under the control of Scer\GAL4elav-C155 and Scer\GAL4VGlut-OK371.
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 hyperfasciculation phenotype seen in the axons of eye photoreceptor cells in ate third instar Sema-1aScer\UAS.cYa; Scer\GAL4GMR.PF larvae is enhanced by Fas2Scer\UAS.cLa - axons are clustered into relatively few large bundles in the lamina and medulla.
Expression of Fas2Scer\UAS.cLa pre- and post-synaptically, under the control of Scer\GAL4A307 in a Nrg849 heterozygous background fails to suppresses the Nrg849 giant synapse physiological phenotype.
Coexpression of RdlScer\UAS.cSa and Fas2Scer\UAS.cLa in the 3 U motorneurons (under the control of eve2xCQ.RC.T:Scer\GAL4 results in the co-arrest of 54% of the intersegmental motor nerves, indicating an enhancement on the ISN phenotype observed in RdlScer\UAS.cSa;eve2xCQ.RC.T:Scer\GAL4 overexpression experiments. Coexpression of RdlScer\UAS.cSa and Fas2Scer\UAS.cLa in the aCC/RP2 axons (under the control of Scer\GAL4eve.RN2 results in the co-arrest of 97% of the intersegmental motor nerves (ISN), indicating an enhancement on the ISN phenotype observed in RdlScer\UAS.cSa;Scer\GAL4eve.RN2 overexpression experiments (where 70% of ISNs are stalled).
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.
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.
The migration phenotypes of border follicle cells in Fas2rd1 homozygotes are rescued by Fas2Scer\UAS.cLa; Scer\GAL4BA3. When Scer\GAL4slbo.2.6 is used instead, the migration rate of the border follicle cells is rescued, but delamination is still delayed, and the border follicle cells lose their polarity.
Expression of Fas2Scer\UAS.cLa under the control of Scer\GAL4hs.PB rescues the genitalia rotation defects seen in Fas2spin males if a single heat shock is given at 7 days of development. If Fas2Scer\UAS.cLa is expressed under the control of Scer\GAL4hs.PB using heat shock applied before or after this period, little rescuing activity of the Fas2spin male genitalia rotation defects is seen. The genitalia rotation defects seen in Fas2spinR5 males are fully rescued by expression of Fas2Scer\UAS.cLa under the control of Scer\GAL4elav.PLu or Scer\GAL4Kurs21. The genitalia rotation defects seen in Fas2spinR5 males are partially rescued by expression of Fas2Scer\UAS.cLa under the control of Scer\GAL4Feb78. The genitalia rotation defects seen in Fas2spinR5 males are not rescued by expression of Fas2Scer\UAS.cLa under the control of Scer\GAL4Feb211 or Scer\GAL4Aug21. Expression of Fas2Scer\UAS.cLa under the control of Scer\GAL4Feb170 either completely rescues or fails to rescue the genitalia rotation defects seen in Fas2spinR5 males (the Scer\GAL4Feb170 allele shows variegated Scer\GAL4 expression).
Lethality of Fas2EB112 is rescued by expression of Fas2Scer\UAS.cLa under the control of Scer\GAL4elav.PLu, Scer\GAL4E62-2 or Scer\GAL4Mhc.PW.
Scer\GAL4 induced expression rescues the lethality of Fas2EB112.
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Mutant
Wild-type
Stocks (0)
Notes on Origin
Discoverer
External Crossreferences and Linkouts ( 0 )
Synonyms and Secondary IDs (3)
Reported As
Symbol Synonym
Fas2Scer\UAS.cLa
Fas2UAS.cLa
Name Synonyms
Saccharomyces cerevisiae UAS construct a of Lin
Secondary FlyBase IDs
    References (27)